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| 13. |
- Benson, Mikael, 1954, et al.
(författare)
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Gene profiling reveals decreased expression of uteroglobin and other anti-inflammatory genes in nasal fluid cells from patients with intermittent allergic rhinitis
- 2005
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Ingår i: Clin Exp Allergy. - : Wiley. ; 35:4, s. 473-478
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Intermittent allergic rhinitis (IAR) results from interactions between a large number of pro- and anti-inflammatory mediators. Little is known about anti-inflammatory mediators in IAR. DNA microarrays allow simultaneous analysis of the whole transcriptome in a sample. OBJECTIVE: To identify anti-inflammatory transcripts in nasal fluid cells from patients with IAR during season and from healthy controls. METHODS: Nasal lavage fluids were obtained from 15 patients with symptomatic birch/and or grass pollen-induced IAR and 28 healthy controls. RNA was extracted from the nasal fluid cells and pooled into one patient- and one control pool. These were analysed with DNA microarrays containing more than 44,927 genes and variants. RESULTS: Seventeen thousand three hundred and fifty three genes were expressed in the controls and 17 928 in the patients. One thousand five hundred and seventy nine of the genes had higher expression in patients than in controls, and 1570 had lower expression in patients. Out of 189 up-regulated inflammatory genes, 187 were pro-inflammatory and two were anti-inflammatory. These genes regulated key steps of inflammation, ranging from influx of leukocytes to immunoglobulin production. By comparison, out of 49 down-regulated inflammatory genes, 36 were pro-inflammatory and 13 were anti-inflammatory. The anti-inflammatory gene that decreased most in expression in the patients was uteroglobin (also known as Clara Cell protein 16, CC16). The nasal fluid concentrations of uteroglobin protein were significantly lower in patients than in controls, 5.43+/-1.53 and 12.93+/-2.53 ng/mL, respectively (P<0.05). CONCLUSION: IAR is associated with decreased expression of uteroglobin and other anti-inflammatory genes.
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| 14. |
- Benson, Mikael, 1954, et al.
(författare)
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Gene profiling reveals increased expression of uteroglobin and other anti-inflammatory genes in glucocorticoid-treated nasal polyps.
- 2004
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Ingår i: Journal of Allergy and Clinical Immunology. - : Elsevier BV. - 0091-6749 .- 1097-6825. ; 113:6, s. 1137-43
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Treatment with local glucocorticoids (GCs) decreases symptoms and the size of nasal polyps. This might depend on the downregulation of proinflammatory genes, as well as the upregulation of anti-inflammatory genes. OBJECTIVE: We sought to identify GC-regulated anti-inflammatory genes in nasal polyps. METHODS: Affymetrix DNA microarrays were used to analyze the expression of 22,283 genes in 4 nasal polyps before and after local treatment with fluticasone (400 microg/d). Expression of uteroglobin and mammaglobin B was analyzed with real-time PCR in 6 nasal polyps and in nasal biopsy specimens from 6 healthy control subjects. RESULTS: Two hundred three genes had changed in expression in treated polyps, and 139 had known functions: 54 genes were downregulated, and 85 were upregulated. Genes associated with inflammation constituted the largest single functional group. These genes affected key steps in inflammation (eg, immunoglobulin production; antigen processing and presentation; and the chemoattraction and activation of granulocytes, T cells, and B cells). Several proinflammatory genes were downregulated. In contrast, some anti-inflammatory genes were upregulated. The gene that increased most in terms of expression was uteroglobin. This was confirmed with real-time PCR. By contrast, expression of uteroglobin was lower in untreated polyps than in healthy nasal mucosa. Immunohistochemical investigation showed staining of uteroglobin in the epithelium and in seromucous glands in control subjects and in nasal polyps. CONCLUSION: Upregulation of anti-inflammatory genes, such as uteroglobin, might contribute to the effects of local treatment with GCs in nasal polyps.
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| 15. |
- Benson, Mikael, 1954, et al.
(författare)
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Inverse relation between nasal fluid Clara Cell Protein 16 levels and symptoms and signs of rhinitis in allergen-challenged patients with intermittent allergic rhinitis.
- 2007
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Ingår i: Allergy. - : Wiley. - 0105-4538 .- 1398-9995. ; 62:2, s. 178-83
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Decreased levels of the anti-inflammatory Clara Cell Protein 16 (CC16) are found in intermittent allergic rhinitis (IAR) and asthma. In asthma this decrease has been associated with hyperreactivity and the A38G single nucleotide polymorphism (SNP). The aim of this study was to examine if IAR is associated with signs and symptoms of rhinitis and the A38G SNP. METHODS: Nasal fluid CC16 was analyzed in 20 patients with IAR before allergen challenge and 1 and 6 h after challenge, and from 28 healthy controls. The A38G SNP was analyzed in 80 patients with IAR and 106 controls. Nasal biopsies were obtained from three subjects in each group for immunohistochemical analysis of CC16. RESULTS: In the allergen-challenged patients symptoms and rhinoscopic signs of rhinitis increased after 1 h and normalized after 6 h. In contrast, nasal fluid CC16 decreased 1 h after allergen challenge and returned to baseline after 6 h. Nasal fluid CC16 levels did not differ from controls before and 6 h after challenge. Immunohistochemical investigation showed intense CC16 staining in the nasal epithelium of both patients before season and healthy controls, but weak staining in symptomatic patients during season. No significant association between the A38G SNP and IAR was found. CONCLUSION: There was an inverse relation between nasal fluid CC16 levels and symptoms and signs of rhinitis in allergen-challenged patients with IAR. However, there was no association between IAR and the A38G SNP.
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| 16. |
- Bogefors, J., et al.
(författare)
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Nod1, Nod2 and Nalp3 receptors, new potential targets in treatment of allergic rhinitis?
- 2010
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Ingår i: Allergy. European Journal of Allergy and Clinical Immunology. - : Wiley-Blackwell. - 0105-4538 .- 1398-9995. ; 65:10, s. 1222-1226
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Recently, a new set of pattern-recognition receptors, the nucleotide-binding oligomerization domain (Nod)-like receptors (NLRs), have emerged. Their activation, either by allergens or microbes, triggers an inflammatory response. The knowledge about NLRs in human airways is limited.AIM OF THE STUDY: To investigate presence of NLRs in the human nose of healthy individuals and patients with intermittent allergic rhinitis outside and during pollen season.METHODS: The expression of Nod1, Nod2, and Nalp3 in nasal biopsies was determined with real-time RT-PCR and immunohistochemistry. Cultured primary human nasal epithelial cells (HNECs) were analyzed using real-time RT-PCR and flow cytometry to further verify the presence of NLRs in the epithelium.RESULTS: Immunohistochemical analysis revealed presence of Nod1, Nod2, and Nalp3 in the nasal epithelium. This was corroborated in cultured HNECs. Patients suffering from symptomatic allergic rhinitis exhibited lower Nod1 and Nalp3 mRNA levels than both controls and patients during pollen season. Nod2 expression was found in all specimens tested, but no differences were seen between the three groups.CONCLUSION: Nod1, Nod2, and Nalp3 receptors were found to be present in the human nose. The expression of Nod1 and Nalp3 were down-regulated during pollen season among patients with allergic rhinitis. This opens up for new insights and novel therapeutic strategies in inflammatory airway disease.
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| 17. |
- Bogefors, Jesper, et al.
(författare)
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Retinoic acid-inducible gene 1-like receptors in the upper respiratory tract.
- 2011
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Ingår i: American Journal of Rhinology & Allergy. - : SAGE Publications. - 1945-8924 .- 1945-8932. ; 25:6, s. 262-267
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Tidskriftsartikel (refereegranskat)abstract
- Retinoic acid-inducible gene 1-like receptors (RLRs) are a novel family of pattern recognition receptors that include retinoic acid-inducible gene 1 (RIG-1), melanoma differentiation-associated gene 5 (MDA-5), and laboratory of genomics and physiology 2 (LGP-2). The knowledge of RLRs and their function in the human airway is limited. This study explores the role of RLRs in the upper respiratory tract.
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| 18. |
- Cardell, Lars-Olaf, et al.
(författare)
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Downregulation of peroxisome proliferator-activated receptors (PPARs) in nasal polyposis
- 2005
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Ingår i: Respiratory Research. - : Springer Science and Business Media LLC. - 1465-9921 .- 1465-993X. ; 6:1
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Tidskriftsartikel (refereegranskat)abstract
- Background: Peroxisome proliferator-activated receptor (PPAR) alpha, beta delta and gamma are nuclear receptors activated by fatty acid metabolites. An anti-inflammatory role for these receptors in airway inflammation has been suggested. Methods: Nasal biopsies were obtained from 10 healthy volunteers and 10 patients with symptomatic allergic rhinitis. Nasal polyps were obtained from 22 patients, before and after 4 weeks of local steroid treatment (fluticasone). Real-time RT-PCR was used for mRNA quantification and immunohistochemistry for protein localization and quantification. Results: mRNA expression of PPAR alpha, PPAR beta delta, PPAR gamma was found in all specimens. No differences in the expression of PPARs were obtained in nasal biopsies from patients with allergic rhinitis and healthy volunteers. Nasal polyps exhibited lower levels of PPAR alpha and PPAR gamma than normal nasal mucosa and these levels were, for PPAR gamma, further reduced following steroid treatment. PPAR gamma immunoreactivity was detected in the epithelium, but also found in smooth muscle of blood vessels, glandular acini and inflammatory cells. Quantitative evaluation of the epithelial immunostaining revealed no differences between nasal biopsies from patients with allergic rhinitis and healthy volunteers. In polyps, the PPAR gamma immunoreactivity was lower than in nasal mucosa and further decreased after steroid treatment. Conclusion: The down-regulation of PPAR gamma, in nasal polyposis but not in turbinates during symptomatic seasonal rhinitis, suggests that PPAR gamma might be of importance in long standing inflammations.
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| 19. |
- Cardell, Lars-Olaf, et al.
(författare)
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Interleukin-1beta up-regulates tumor necrosis factor receptors in the mouse airways.
- 2008
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Ingår i: Pulmonary Pharmacology & Therapeutics. - : Elsevier BV. - 1522-9629 .- 1094-5539. ; May 2, s. 675-681
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Tidskriftsartikel (refereegranskat)abstract
- Cytokines like interleukin-1beta (IL-1beta) and tumor necrosis factor alpha (TNFalpha), released during the inflammatory process, play important roles in the development of airway hyperresponsiveness. The effects of these cytokines are mediated by cell surface receptors, specific for each cytokine. The expression of cytokine receptors is a dynamic process, where receptors can be up- or down-regulated in response to changes in the environment. One such environmental factor is the presence of cytokines per se. The present study was designed to evaluate the effects of IL-1beta on the expression of its corresponding receptor IL-1 RI, as well as on the closely related TNFalpha receptors TNF RI and TNF RII in airways using a mouse organ culture assay and intranasal inoculation model. Immunohistochemical staining was used to quantify expressional differences between fresh and cultured tracheal segments. In the fresh, uncultured, segments, IL-1 RI and TNF RI were seen in the epithelial layer and TNF RI in the smooth muscle layer. After 4 days of culture, the expression of TNF RI decreased in the epithelial layer, whereas the corresponding expression of IL-1 RI and TNF RI in the smooth muscle remained unchanged. When culture was performed in the presence of IL-1beta, the expression of IL-1 RI and TNF RI in the epithelial cells and TNF RI in the smooth muscle cells increased. TNF RII was not detected in either fresh or cultured trachea, but after treatment with IL-1beta an expression was found in both the epithelial layer and in the smooth muscle cells. The IL-1beta-induced increased expression, on TNF RI and TNF RII in the smooth muscle ex vivo and in the lung parenchyma after intranasal challenge in vivo, was verified at the mRNA level using real-time RT PCR. To summarize, presence of IL-1beta increases the expression of IL-1 R1 and TNF RI and induces expression of TNF RII in the airway wall. It is not inconceivable that these alterations of the IL-1 and TNF receptors may have important functional implications for the development of hyperresponsiveness in inflammatory airway diseases like asthma.
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| 21. |
- Edvinsson, Lars, et al.
(författare)
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Neurobiology in primary headaches.
- 2005
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Ingår i: Brain Research Reviews. - : Elsevier BV. - 1872-6321 .- 0165-0173. ; 48:3, s. 438-456
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Forskningsöversikt (refereegranskat)abstract
- Primary headaches such as migraine and cluster headache are neurovascular disorders. Migraine is a painful, incapacitating disease that affects a large portion of the adult population with a substantial economic burden on society. The disorder is characterised by recurrent unilateral headaches, usually accompanied by nausea, vomiting, photophobia, and/or phonophobia. A number of hypothesis have emerged to explain the specific causes of migraine. Current theories suggest that the initiation of a migraine attack involves a primary central nervous system (CNS) event. It has been suggested that a mutation in a calcium gene channel renders the individual more sensitive to environmental factors, resulting in a wave of cortical spreading depression when the attack is initiated. Genetically, migraine is a complex familial disorder in which the severity and the susceptibility of individuals are most likely governed by several genes that vary between families. Genom wide scans have been performed in migraine with susceptibility regions on several chromosomes some are associated with altered calcium channel function. With positron emission tomography (PET), a migraine active region has been pointed out in the brainstem. In cluster headache, PET studies have implicated a specific active locus in the posterior hypothalamus. Both migraine and cluster headache involve activation of the trigeminovascular system. In support, there is a clear association between the head pain and the release of the neuropeptide calcitonin gene-related peptide (CGRP) from the trigeminovascular system. In cluster headache there is, in addition, release of the parasympathetic neuropeptide vasoactive intestinal peptide (VIP) that is coupled to facial vasomotor symptoms. Triptan administration, activating the 5-HT1B/ (ID) receptors, causes the headache to subside and the levels of neuropeptides to normalise, in part through presynaptic inhibition of the cranial sensory nerves. These data suggest a central role for sensory and parasympathetic mechanisms in the pathophysiology of primary headaches. The positive clinical trial with a CGRP receptor antagonist offers a new promising way of treatment.
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| 23. |
- Fransson, Mattias, et al.
(författare)
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Expression of Toll-like receptor 9 in nose, peripheral blood and bone marrow during symptomatic allergic rhinitis.
- 2007
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Ingår i: Respiratory research. - : Springer Science and Business Media LLC. - 1465-993X .- 1465-9921. ; 8
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Allergic rhinitis is an inflammatory disease of the upper airway mucosa that also affects leukocytes in bone marrow and peripheral blood. Toll-like receptor 9 (TLR9) is a receptor for unmethylated CpG dinucleotides found in bacterial and viral DNA. The present study was designed to examine the expression of TLR9 in the nasal mucosa and in leukocytes derived from different cellular compartments during symptomatic allergic rhinitis. METHODS: The study was based on 32 patients with seasonal allergic rhinitis and 18 healthy subjects, serving as controls. Nasal biopsies were obtained before and after allergen challenge. Bone marrow, peripheral blood and nasal lavage fluid were sampled outside and during pollen season. The expression of TLR9 in tissues and cells was analyzed using immunohistochemistry and flow cytometry, respectively. RESULTS: TLR9 was found in several cell types in the nasal mucosa and in different leukocyte subpopulations derived from bone marrow, peripheral blood and nasal lavage fluid. The leukocyte expression was generally higher in bone marrow than in peripheral blood, and not affected by symptomatic allergic rhinitis. CONCLUSION: The widespread expression of TLR9 in the nasal mucosa along with its rich representation in leukocytes in different compartments, demonstrate the possibility for cells involved in allergic airway inflammation to directly interact with bacterial and viral DNA.
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| 24. |
- Fransson, Mattias, et al.
(författare)
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Lipopolysaccharide-induced down-regulation of uteroglobin in the human nose.
- 2007
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Ingår i: Acta Oto-Laryngologica. - : Informa UK Limited. - 1651-2251 .- 0001-6489. ; 127:3, s. 285-291
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Tidskriftsartikel (refereegranskat)abstract
- Conclusion. Lipopolysaccharide (LPS) challenge of the human nose has the capacity to reduce the amount of natural anti-inflammatory proteins, such as uteroglobin. Objectives. Nasal challenge with LPS, an activator of innate immunity, has been shown to increase the amount of pro-inflammatory mediators in nasal lavage fluid. Uteroglobin is a newly described anti-inflammatory mediator that is secreted in the nose. This study examined the effect of nasal LPS application on the level of uteroglobin in nasal lavage fluid as well as on the expression of uteroglobin in nasal mucosa. Materials and methods. Thirty-eight volunteers were challenged nasally with either 50 mu g LPS or vehicle; 6 h later, nasal lavage fluid was collected and a nasal biopsy was obtained. Levels of uteroglobin, albumin and the pro-inflammatory mediators interleukin (IL)-6 and IL-8 were analysed in the lavage fluids using enzyme-linked immunosorbent assays (ELISAs). Biopsies were used for either quantification of uteroglobin mRNA by real-time PCR or for localization of the corresponding protein with immunohistochemistry. Results. The uteroglobin level decreased in nasal lavage fluid following LPS challenge, whereas the levels of IL-6 and albumin increased. Uteroglobin was mainly seen in the respiratory epithelium and its mRNA expression decreased as a consequence of the LPS challenge.
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| 25. |
- Fransson, Mattias, et al.
(författare)
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Up-regulation of Toll-like receptors 2, 3 and 4 in allergic rhinitis
- 2005
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Ingår i: Respiratory Research. - : Springer Science and Business Media LLC. - 1465-9921 .- 1465-993X. ; 6:100
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Toll-like receptors enable the host to recognize a large number of pathogen-associated molecular patterns such as bacterial lipopolysaccharide, viral RNA, CpG-containing DNA and flagellin. Toll-like receptors have also been shown to play a pivotal role in both innate and adaptive immune responses. The role of Toll-like receptors as a primary part of our microbe defense system has been shown in several studies, but their possible function as mediators in allergy and asthma remains to be established. The present study was designed to examine the expression of Toll-like receptors 2, 3 and 4 in the nasal mucosa of patients with intermittent allergic rhinitis, focusing on changes induced by exposure to pollen. METHODS: 27 healthy controls and 42 patients with seasonal allergic rhinitis volunteered for the study. Nasal biopsies were obtained before and during pollen season as well as before and after allergen challenge. The seasonal material was used for mRNA quantification of Toll-like receptors 2, 3 and 4 with real-time polymerase chain reaction, whereas specimens achieved in conjunction with allergen challenge were used for immunohistochemical localization and quantification of corresponding proteins. RESULTS: mRNA and protein representing Toll-like receptors 2, 3 and 4 could be demonstrated in all specimens. An increase in protein expression for all three receptors could be seen following allergen challenge, whereas a significant increase of mRNA only could be obtained for Toll-like receptor 3 during pollen season. CONCLUSION: The up-regulation of Toll-like receptors 2, 3 and 4 in the nasal mucosa of patients with symptomatic allergic rhinitis supports the idea of a role for Toll-like receptors in allergic airway inflammation.
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| 26. |
- Granath, Anna, et al.
(författare)
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Increased TLR7 expression in the adenoids among children with otitis media with effusion
- 2010
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Ingår i: Acta Oto-Laryngologica. - : Informa UK Limited. - 1651-2251 .- 0001-6489. ; 130:1, s. 57-61
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Tidskriftsartikel (refereegranskat)abstract
- Conclusion: Toll-like receptor 7 (TLR7) is present in the adenoids in young children and might play a role in the immunological response behind the development of otitis media with effusion (OME). Objectives: To investigate the expression of the TLRs TLR4 and TLR7 in adenoids from children with OME and to compare the results with data obtained from healthy controls. Subjects and methods: This was a controlled, prospective study. Eleven young children with long-standing OME and 10 controls with healthy middle ears were recruited consecutively when scheduled for adenoidectomy. mRNA was quantified using real-time polymerase chain reaction (PCR) and the localization of the corresponding proteins was assessed by immunohistochemistry. Results: mRNA for TLR4 and TLR7 could be obtained from all samples tested along with their corresponding proteins. The mRNA levels for TLR7 were increased among the children with a history of OME. No such increase was found for TLR4.
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| 27. |
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| 28. |
- Granath, Anna, et al.
(författare)
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Reduced iNOS expression in adenoids from children with otitis media with effusion.
- 2010
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Ingår i: Pediatric allergy and immunology : official publication of the European Society of Pediatric Allergy and Immunology. - : Wiley. - 1399-3038. ; 21:8, s. 1151-1156
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Tidskriftsartikel (refereegranskat)abstract
- Granath A, Norrby-Teglund A, Uddman R, Cardell L-O. Reduced iNOS expression in adenoids from children with otitis media with effusion. Pediatr Allergy Immunol 2010: 21: 1151-1156. © 2010 John Wiley & Sons A/S Nitric oxide (NO) is a key mediator in the local immune response of human airways. Inducible NO-synthases (iNOS), and endothelial NO-synthases (eNOS) are two enzymes known to regulate its production. The role of NO in middle ear disease is not fully known. Previous studies suggest that NO might have a dual role, both promoting and suppressing middle ear inflammation. The aim of the present study was to compare the eNOS and iNOS expression in adenoids obtained from children with otitis media with effusion (OME) with the expression seen in adenoids derived from children without middle ear disease. In addition, the expression of IL-1β and TNF-α were analyzed, because of their role in the iNOS-induction pathway. The iNOS and eNOS expression were analyzed with real-time PCR in 8 OME and 11 control adenoids. The corresponding proteins were demonstrated by immunohistochemical staining of adenoid tissue. A Luminex(®) assay was performed to analyze IL-1β and TNF-α in nasopharyngeal secretion in 10 OME and 8 controls, and immunohistochemistry was performed on adenoid tissue and imprints from the adenoid surface. Children with OME exhibited lower levels of iNOS than controls without middle ear disease. No such difference was seen for eNOS. The corresponding proteins were found mainly in conjunction with surface epithelium. No significant changes were seen among the cytokines tested. The present results indicate that local induction of iNOS in adenoids might be of importance for preventing development of OME.
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| 29. |
- Hellstrand, Per, et al.
(författare)
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Role of vasoactive intestinal polypeptide (VIP) in the neurogenic vasodilatation of the portal vein in the rabbit
- 1985
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Ingår i: Regulatory Peptides. - : Elsevier BV. - 1873-1686 .- 0167-0115. ; 12:4, s. 309-316
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Tidskriftsartikel (refereegranskat)abstract
- A coarse network of nerve fibres displaying immunoreactivity for vasoactive intestinal polypeptide (VIP) was found in the wall of the hepatic portal vein of the rabbit. Electrical field stimulation of the rabbit portal vein in vitro, in the presence of adrenergic and cholinergic blockade, caused a marked relaxation of the vessel and a release of VIP into the perfusate. Addition of VIP to the tissue bath elicited a concentration-dependent inhibition of the mechanical activity of the portal vein. The results suggest that VIP containing neurones might participate in the non-cholinergic, non-adrenergic vasodilatation of the portal vein in the rabbit.
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| 30. |
- Hou, Mingyan, et al.
(författare)
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Capsaicin receptor immunoreactivity in the human trigeminal ganglion.
- 2002
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Ingår i: Neuroscience Letters. - 0304-3940. ; 330:3, s. 223-226
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Tidskriftsartikel (refereegranskat)abstract
- The cloned capsaicin receptor, also known as vanilloid receptor subtype 1 (VR1) receptor, has been demonstrated to be an integral membrane protein with homology to a family of putative store-operated calcium channels. The VR1 receptor is activated not only by capsaicin but also by noxious heat and protons, and therefore it is suggested as a molecular integrator of chemical and physical stimuli that elicit pain. In the present study, indirect immunofluorescence detected a small number of neurons that are VR1 receptor immunoreactive (ir) (171 versus 1038 or 16% of all neuronal cell bodies) in the human trigeminal ganglion (TG). In addition, RT-PCR confirmed the presence of VR1 mRNA in the human TG. It has been hypothesized that TG neuronal cell bodies are the source of capsaicin-stimulated release of calcitonin gene-related peptide (CGRP), and hence co-localization experiments were performed. Around 10% of the VR1 receptor-ir is expressed on neurons that contain CGRP-ir (ten among 74) in the human TG, indicating that capsaicin may act through the VR1 receptor to modulate the release of CGRP and in turn to modulate pain. We observed that 8% of the VR1 receptor-ir neuronal cell bodies contain substance P-ir and 5% nitric oxide synthase. Capsaicin can release nitric oxide, CGRP and substance P from sensory nerves and contribute to central sensitization.
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| 31. |
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| 32. |
- Kinhult, Johan, et al.
(författare)
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Increased expression of surface activation markers on neutrophils following migration into the nasal lumen
- 2003
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Ingår i: Clinical and Experimental Allergy. - : Wiley-Blackwell. - 0954-7894 .- 1365-2222. ; 33:8, s. 1141-1146
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: The sequence of events following the recruitment of a free-flowing neutrophil in the peripheral circulation, via adhesion, migration and release of mediators, to a neutrophil on the surface of the nasal epithelium is a co-ordinated process. Little is known about the state of neutrophil activation following this course of events.OBJECTIVES: To investigate the expression of surface activation markers on neutrophils, reflecting activation during their recruitment to the nose, and to see whether the inflammatory process during allergic rhinitis influences this process.METHOD: Nine healthy controls and 12 patients with grass pollen-induced intermittent allergic rhinitis were investigated during the peak of the pollen season. The expression of CD11b, CD66b and CD63 on the neutrophil cell surface, as a reflection of activation, was analysed using flow cytometry. Neutrophils were derived from peripheral blood and nasal lavage fluid. In addition, eosinophil cationic protein (ECP) and myeloperoxidase (MPO) as well as L-, P- and E-selectins in the nasal lavage fluid were analysed using RIA and ELISA, respectively.RESULTS: A marked increase in the expression of all three CD markers on the neutrophil cell surface was noticed following migration from the bloodstream to the surface of the nasal mucosa. At the peak of the grass pollen season, the MPO levels increased, reflecting an increase in the total number of nasal fluid neutrophils. In parallel, the expression of CD11b was further augmented. The expression of the CDb11b was reduced on neutrophils remaining in the circulation. In addition, the level of L-selectin was reduced on neutrophils derived from the blood during allergic inflammation.CONCLUSION: Neutrophils might become activated during their transfer from the blood to the surface of the nasal mucosa, but these changes may also be due to depletion of activated neutrophils in the blood via activated endothelial/epithelial adhesion and chemoattractant measures. The increased expression of surface activation markers during allergic rhinitis suggests roles for neutrophils in the inflammatory process.
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| 33. |
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| 34. |
- Kuris, Aniko, et al.
(författare)
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Enhanced expression of CGRP in rat trigeminal ganglion neurons during cell and organ culture
- 2007
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Ingår i: Brain Research. - : Elsevier BV. - 1872-6240 .- 0006-8993. ; 1173, s. 6-13
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Tidskriftsartikel (refereegranskat)abstract
- The sensory innervation of intracranial vessels originates in the trigeminal ganglion with calcitonin gene-related peptide (CGRP), substance P (SP) and pituitary adenylate cyclase activating peptide (PACAP) as frequent neuronal messengers. The present study was designed to study the expression of these neuropeptides (a) in primary culture of adult rat trigeminal ganglion neuronal cells and (b) in organ culture of sections of the trigeminal ganglion. In cell culture, axons grow in the peripheral direction for up to 48 h. Immunocytochemistry revealed that the cell bodies showed increased expression of CGRP at 24 h and SP at 24-48 h (p < 0.05), whereas cell culture did not increase the expression of PACAP at 24 h (p>0.05), but at 48 h (p<0.05). A significant elevation of CGRP mRNA was seen at 12 h, i.e. before the increased CGRP immunoreaction was observed. In organ culture of sections of trigeminal ganglia, the number of CGRP immunoreactive (-ir) cells and the mRNA expression were significantly increased at 24 and 48 h of incubation as compared to control (p<0.05), while the number of SP-ir cells was not altered (p>0.05). In conclusion, neurons of rat trigeminal ganglia alter their expression of neuropeptides during cell and organ culture differently, but it is mainly the CGRP system that is up-regulated. We have compared two methods for future studies of underlying molecular mechanisms responsible for regulation of neuropeptide expression in the trigeminal system. (C) 2007 Elsevier B.V. All rights reserved.
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| 35. |
- Larsson, Olivia, et al.
(författare)
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Substance P represents a novel first-line defense mechanism in the nose
- 2018
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Ingår i: Journal of Allergy and Clinical Immunology. - : Elsevier BV. - 0091-6749 .- 1097-6825. ; 141:1, s. 3-136
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Tidskriftsartikel (refereegranskat)abstract
- Background: Neuropeptides, such as substance P (SP), have long been seen as mediators of widespread continuous airway inflammation, a process known as neurogenic inflammation. However, this has been difficult to demonstrate clinically, suggesting an alternative role for these signaling molecules. Objectives: We sought to examine the role of SP in nasal infection by assessing the release of SP in response to viral stimulation and characterizing the effects of SP on innate immunity, with the latter reflected in changes in local Toll-like receptor (TLR) expression. Methods: The distribution of SP and TLRs in the nasal mucosa and local airway neurons was assessed with immunohistochemistry. The TLR7 agonists R-837 and R-848 were used to mimic a viral insult in the upper airways represented by primary human nasal epithelial cells (HNECs) and murine nasal epithelial cells (MNECs) and isolated murine trigeminal ganglial neurons. SP release from HNECs, MNECs, and trigeminal ganglial neurons was quantified with EIA. The effects of SP on TLR expression on HNECs were determined by using flow cytometry and confocal microscopy. Results: SP was released from the sensory neurons, MNECs, and HNECs within 15 minutes of local TLR7 stimulation. Subsequently, stimulation with SP induced upregulation of TLR expression in HNECs within 30 minutes through induction of TLR movement within HNECs. Upregulation of TLR expression was not evident when cells were treated with the neurokinin 1 receptor antagonist aprepitant before SP stimulation. Conclusions: This highlights a novel role for sensory neuropeptides as acute and local mediators of pathogen-driven inflammation, rapidly priming innate immune defenses in the airway.
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| 36. |
- Lindberg, Sven, et al.
(författare)
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VIP potentiates cholinergic effects on the mucociliary system in the maxillary sinus
- 1988
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Ingår i: Otolaryngology: Head and Neck Surgery. - 0194-5998. ; 99:4, s. 401-407
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Tidskriftsartikel (refereegranskat)abstract
- The neuropeptide vasoactive intestinal polypeptide (VIP), which is found in a population of cholinergic parasympathetic neurons in the airways, has no effects per se on mucociliary activity. In order to test the hypothesis that VIP may modulate cholinergic regulation of the mucociliary system, VIP was infused intraarterially (8.4 pmol/kg/min), and the response to challenges with methacholine in the maxillary sinus of rabbits were recorded with a photoelectric technique. Occurrence of VIP-like immunoreactivity in the rabbit maxillary sinus, maxillary nerve, and sphenopalatine ganglion was investigated. Immunoreactivity against VIP was found in nerve fibers in the subepithelial layer of the maxillary sinus and in numerous nerve cell bodies in the sphenopalatine ganglion. Infusion of VIP potentiated the mucociliary increase induced by methacholine. The mucociliary wave frequency change increased from 6.1% +/- 1.7% to 13.3% +/- 3.9% (0.01 micrograms/kg methacholine), from 11.6% +/- 3.6% to 18.8% +/- 2.2% (0.05 micrograms/kg) and from 17.0% +/- 3.0% to 27.4% +/- 3.6% (0.1 micrograms/kg). Both peak responses and response durations increased during infusions. In contrast, the vasodilating agent papaverine sulphate did not influence the mucociliary response to methacholine. The modulating effect of VIP on the mucociliary system, taken together with the morphologic observations, suggest that VIP may have a physiologic role in the regulation of the mucociliary system in the maxillary sinus.
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| 37. |
- Mansson Kvarnhammar, Anne, et al.
(författare)
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Diminished levels of nasal S100A7 (psoriasin) in seasonal allergic rhinitis: an effect mediated by Th2 cytokines
- 2012
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Ingår i: Respiratory Research. - : BioMed Central. - 1465-9921 .- 1465-993X. ; 13:2
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Tidskriftsartikel (refereegranskat)abstract
- Background: S100A7 is an antimicrobial peptide involved in several inflammatory diseases. The aim of the present study was to explore the expression and regulation of S100A7 in seasonal allergic rhinitis (SAR). less thanbrgreater than less thanbrgreater thanMethods: Nasal lavage (NAL) fluid was obtained from healthy controls before and after lipopolysaccharide (LPS) provocation, from SAR patients before and after allergen challenge, and from SAR patients having completed allergen-specific immunotherapy (ASIT). Nasal biopsies, nasal epithelial cells and blood were acquired from healthy donors. The airway epithelial cell line FaDu was used for in vitro experiments. Real-time RT-PCR and immunohistochemistry were used to determine S100A7 expression in nasal tissue and cells. Release of S100A7 in NAL and culture supernatants was measured by ELISA. The function of recombinant S100A7 was explored in epithelial cells, neutrophils and peripheral blood mononuclear cells (PBMC). less thanbrgreater than less thanbrgreater thanResults: Nasal administration of LPS induced S100A7 release in healthy non-allergic subjects. The level of S100A7 was lower in NAL from SAR patients than from healthy controls, and it was further reduced in the SAR group 6 h post allergen provocation. In contrast, ASIT patients displayed higher levels after completed treatment. S100A7 was expressed in the nasal epithelium and in glands, and it was secreted by cultured epithelial cells. Stimulation with IL-4 and histamine repressed the epithelial S100A7 release. Further, recombinant S100A7 induced activation of neutrophils and PBMC. less thanbrgreater than less thanbrgreater thanConclusions: The present study shows an epithelial expression and excretion of S100A7 in the nose after microbial stimulation. The levels are diminished in rhinitis patients and in the presence of an allergic cytokine milieu, suggesting that the antimicrobial defense is compromised in patients with SAR.
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| 38. |
- Millrud, Camilla Rydberg, et al.
(författare)
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Nod-like receptors in head and neck squamous cell carcinoma
- 2013
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Ingår i: Acta Oto-Laryngologica. - : Informa UK Limited. - 1651-2251 .- 0001-6489. ; 133:12, s. 1333-1344
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Tidskriftsartikel (refereegranskat)abstract
- Conclusion: The capability of Nod1 to recognize bacteria along with its altered expression and ability to cause an immunological response in head and neck cancer suggest a novel pathway for bacteria to interfere with ongoing cancer inflammation. Objective: Nucleotide oligomerization domain (Nod)-like receptors (NLRs) comprise a recently discovered family of pattern-recognition receptors. In addition to their protective function against infections, accumulating evidence suggests a role for these receptors in various diseases, including cancer. The present study was designed to explore the presence of NLRs in head and neck squamous cell carcinoma, and to determine if these cells have the ability to respond immunologically to ligand stimulation. Methods: The pharyngeal squamous cell carcinoma cell lines Detroit-562 and FaDu were used as a model for head and neck cancer, and compared to healthy primary human nasal epithelial cells. Analyses were performed using immuno-histochemistry, real-time RT-PCR, Luminex Multiplex Immunoassay, ELISA, and flow cytometry. Results: The expression profile of NLRs in head and neck cancer cells differed from that seen in healthy epithelial cells. Further, Nod1 stimulation induced an immunological response in tumor cells that differed from the response in normal epithelial cells, especially regarding the expression of beta-defensin 2, granulocyte monocyte colony stimulating factor (GM-CSF), granulocyte colony stimulating factor (G-CSF), intercellular adhesion molecule-1 (ICAM-1), and cell survival.
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| 39. |
- Mork, H, et al.
(författare)
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Does nociceptin play a role in pain disorders in man?
- 2002
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Ingår i: Peptides. - 1873-5169. ; 23:9, s. 1581-1587
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Tidskriftsartikel (refereegranskat)abstract
- Nociceptin-immunoreactive cellbodies were detected in the human trigeminal ganglion, while no such fibers were identified in the temporal artery or in dermal tissue from the neck region. In four healthy subjects receiving nociceptin into the temporal muscle in an open labeled design no pain was detected. In 10 healthy subjects who received 200 pmol of nociceptin into tender non-dominant trapezius muscles in a placebo-controlled, randomized, balanced, and double-blinded design local tenderness increased (P = 0.025) while no pain was noted. Thus, the action of nociceptin should be searched for in the trigeminal ganglion and/or in the central nervous system (CNS). (C) 2002 Elsevier Science Inc. All rights reserved.
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| 40. |
- Månsson, Anne, et al.
(författare)
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NOD-like receptors in the human upper airways: a potential role in nasal polyposis.
- 2011
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Ingår i: Allergy. - : Wiley. - 1398-9995 .- 0105-4538. ; 66, s. 621-628
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Tidskriftsartikel (refereegranskat)abstract
- To cite this article: Månsson A, Bogefors J, Cervin A, Uddman R, Cardell LO. NOD-like receptors in the human upper airways: a potential role in nasal polyposis. Allergy 2010; DOI: 10.1111/j.1398-9995.2010.02527.x. ABSTRACT: Background: Nucleotide-binding oligomerization domain (NOD)-like receptors (NLRs) are newly discovered cytosolic receptors belonging to the pattern-recognition receptor family. They detect various pathogen-associated molecular patterns, triggering an immune response. The knowledge about these receptors, and their role in health and disease, is limited. The aim of the present study was to characterize the expression of NOD1, NOD2, and NALP3 in the human upper airways. Methods: Surgical samples were obtained from patients with tonsillar disease (n = 151), hypertrophic adenoids (n = 9), and nasal polyposis (n = 24). Nasal biopsies were obtained from healthy volunteers (n = 10). The expression of NOD1, NOD2, and NALP3 was analyzed using real-time PCR and immunohistochemistry. Results: Expression of NOD1, NOD2, and NALP3 mRNA and protein were seen in all tissue specimens. The NLR mRNA was found to be higher in nasal polyps than in normal nasal mucosa, and local steroid treatment reduced the NLR expression in polyps. In contrast, tonsillar infection with Streptococcus pyogenes or Haemophilus influenzae did not affect the NLR expression. Conclusions: The present study demonstrates the presence of NLRs in several upper airway tissues and highlights a potential role of NLRs in chronic rhinosinusitis with polyps.
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| 41. |
- Månsson, Anne, et al.
(författare)
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TLR3 in human eosinophils: functional effects and decreased expression during allergic rhinitis.
- 2010
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Ingår i: International archives of allergy and immunology. - : S. Karger AG. - 1423-0097 .- 1018-2438. ; 151:2, s. 118-28
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND/AIM: Viral respiratory infections are increasingly implicated in allergic exacerbations. Virus-induced activation of eosinophils through Toll-like receptors (TLRs) could be involved. The present study was designed to examine TLR3 expression in eosinophils from bone marrow (BM) and peripheral blood (PB) during symptomatic allergic rhinitis, and to evaluate the functional responsiveness of TLR3 in purified eosinophils. METHODS: BM and PB samples were obtained from healthy volunteers and patients with seasonal allergic rhinitis outside and during the pollen season. Eosinophils were analyzed for TLR3 expression by flow cytometry. Polyinosinic:polycytidylic acid [poly(I:C)], an agonist for TLR3, was used to assess its functional role in purified eosinophils and the intracellular signaling pathways involved. RESULTS: TLR3 expression was demonstrated in BM and PB eosinophils. It was higher in BM-derived than in circulating cells and it was downregulated in both compartments during symptomatic allergic rhinitis. TLR3 expression was also downregulated in the presence of interleukin (IL)-4 and IL- 5. Stimulation with poly(I:C) increased the percentage of CD11b+ cells and enhanced the secretion of IL-8, effects mediated via the p38 mitogen-activated protein kinases and nuclear factor-kappaB signaling pathways. Moreover, pretreatment with IL-5 augmented the poly(I:C)-induced IL-8 release. CONCLUSIONS: Eosinophils activated via TLR3 might be more able to home and recruit leukocytes to sites of inflammation. The decreased TLR3 expression during symptomatic allergic rhinitis and in the presence of Th2 cytokines indicates a role in allergic airway inflammation. Thus, eosinophils might function as a link between viral infections and exacerbations of allergic disease.
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| 42. |
- Runer, Thomas, et al.
(författare)
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Nitric oxide is a regulator of mucociliary activity in the upper respiratory tract
- 1998
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Ingår i: Otolaryngology: Head and Neck Surgery. - 0194-5998. ; 119:3, s. 278-287
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Tidskriftsartikel (refereegranskat)abstract
- The in vitro effects of the nitric oxide (NO) substrate L-arginine on ciliary beat frequency and the in vivo effects of the NO donor sodium nitroprusside (SNP) on mucociliary activity were investigated in the rabbit maxillary sinus mucosa with photoelectric techniques. L-Arginine increased ciliary beat frequency in vitro with a maximum response of 27.1% +/- 6.4% at 10(-3) mol/L, and this effect was reversibly blocked by pretreatment with the NO synthase (NOS) inhibitor N(G)-nitro-L-arginine, whereas D-arginine had no such effect. SNP increased mucociliary activity in vivo, the peak response of 36.8% +/- 4.2% being obtained at the dose of 30.0 microg/kg. No tachyphylaxis was observed after repeat challenge with SNP. The increase in mucociliary activity caused by SNP was largely unaffected by pretreatment with the calcium channel blocker nifedipine, the cyclooxygenase inhibitor diclofenac, and the cholinergic antagonist atropine. The nonselective beta-blocker propranolol delayed the peak response of SNP to 7 to 8 minutes after challenge, compared with 1 to 2 minutes after challenge in animals without pretreatment. The results show the NO substrate L-arginine and the NO donor SNP to have ciliostimulatory effects in vitro and in vivo, respectively. The occurrence of NOS production in the sphenopalatine ganglion and sinus mucosa of the rabbit was studied by immunohistochemistry for NOS activity or nicotinamide adenine dinucleotide phosphate-diaphorase histochemistry. The latter is an indirect sign of neuronal NOS activity. Numerous NOS-containing cell bodies were seen in the sphenopalatine ganglion; in the sinus mucosa a moderate supply of thin NOS-immunoreactive nerve fibers was seen. Taken together, the morphologic findings and the functional results indicate NO to be a regulator of mucociliary activity in upper airways.
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| 43. |
- Rydberg, Camilla, et al.
(författare)
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Toll-like receptor agonists induce inflammation and cell death in a model of head and neck squamous cell carcinomas
- 2009
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Ingår i: Immunology. - : Wiley. - 0019-2805 .- 1365-2567. ; 128:1, s. 600-611
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Tidskriftsartikel (refereegranskat)abstract
- P>Toll-like receptors (TLRs) are increasingly implicated in the pathogenesis of cancer. The present study describes TLR expression and function in healthy and malignant airway epithelial cells. The squamous cell carcinoma cell line Detroit-562 was compared with the healthy bronchial epithelial cell line NL-20 and primary human nasal epithelial cells (HNECs). TLR2, TLR3 and TLR5 were present in primary head and neck squamous cell carcinomas (HNSCCs). Consistent with this, Detroit-562 expressed TLR2, TLR3 and TLR5, whereas NL-20 expressed mainly TLR3 and HNECs expressed TLR2-5. In Detroit-562, Pam(3)CSK(4), poly(I:C) and flagellin, ligands for TLR2, TLR3 and TLR5, respectively, induced an up-regulation of intercellular adhesion molecule 1 (ICAM-1), an increase in interleukin (IL)-6 and IL-8 secretion and a decrease in cell viability. Additionally, poly(I:C) affected IL-1 beta production and the migratory behaviour of Detroit-562. NL-20 responded with a slight increase in IL-8 secretion upon poly(I:C) stimulation. Poly(I:C) induced a small increase in IL-1 beta, IL-6 and IL-8 production in HNECs, while Pam(3)CSK(4) increased viability. The TLR signalling was transcription-dependent, but the pathways involved differed among TLRs as well as cells. In Detroit-562, TLR2 and TLR5 activation was mediated via c-jun N-terminal kinase (JNK)-, p38-, phosphatidylinositol 3-kinase (PI3K)- and nuclear factor (NF)-kappa B-related pathways, while TLR3 was dependent on NF-kappa B. In NL-20, TLR3 signalled via p38, and in HNECs, NF-kappa B, JNK and extracellular signal-regulated kinase (ERK) appeared to be involved. We found that TLR agonists induced a robust response in HNSCCs, characterized by generation of inflammation and cell death. A similar response was not seen in normal epithelial cells. Thus, the TLR system should be considered an important target in future antitumour immunotherapy.
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| 44. |
- Rydberg Millrud, Camilla, et al.
(författare)
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The Activation Pattern of Blood Leukocytes in Head and Neck Squamous Cell Carcinoma Is Correlated to Survival
- 2012
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Ingår i: PLoS ONE. - : Public Library of Science (PLoS). - 1932-6203. ; 7:12
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Tidskriftsartikel (refereegranskat)abstract
- Head and neck squamous cell carcinoma (HNSCC) is known to cause substantial immunosuppression. The present study was designed to characterize blood leukocyte activation in HNSCC and to investigate if the individual activation pattern could be related to tumor progress and survival. The leukocyte activation profile of HNSCC patients and healthy controls was assessed with flow cytometry. HNSCC patients displayed increased numbers of monocytes, neutrophils and total leukocytes as well as an enhanced neutrophil/lymphocyte ratio. In addition, patients had a higher percentage of CD69(+), CD71(+) and CD98(+) T cell subsets and NK cells, and a reduced expression of L-selectin in CD14(high)CD16(+) monocytes and neutrophils, when compared to controls. These changes could be correlated to both tumor burden and spread to lymph nodes. Among the cancer patients an increased neutrophil/lymphocyte ratio, a low neutrophil and CD14(high) CD16(+) monocyte activation state and an elevated CD4/CD8 ratio were related to poor survival. In contrast, a high percentage of CD98(+) Th cells appeared to be associated with a better outcome. Taken together, the present data indicate that HNSCC causes activation of blood leukocytes and that the individual activation pattern can be linked to prognosis.
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| 45. |
- Uddman, Rolf, et al.
(författare)
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Neuropeptide-containing nerve fibers in the pharynx of the rabbit
- 1990
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Ingår i: Dysphagia. - 1432-0460. ; 4:4, s. 220-226
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Tidskriftsartikel (refereegranskat)abstract
- The distribution of peptide-containing nerve fibers in the pharyngeal region of rabbits was studied by immunocytochemistry. Neuropeptide Y (NPY)-containing fibers were numerous around blood vessels and moderate in number among bundles of striated muscle fibers. A few NPY-containing fibers were seen around seromucous glands and beneath the epithelium. Nerve fibers containing vasoactive intestinal peptide (VIP) were numerous around seromucous glands and moderate in number around blood vessels, bundles of muscle, and in the subepithelial layer. A few nerve fibers containing substance P (SP) were seen around blood vessels, seromucous glands, among bundles of muscle, and in the subepithelial layer. Nerve fibers containing calcitonin gene-related peptide (CGRP) were numerous. They were distributed close to blood vessels, among bundles of muscle, in the subepithelial layer, and within the epithelium. A conspicuous finding was the occurrence of CGRP within motor end plates of striated muscle.
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| 46. |
- Uddman, Rolf, et al.
(författare)
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Neuropeptide expression in the human trigeminal nucleus caudalis and in the cervical spinal cord C1 and C2.
- 2002
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Ingår i: Cephalalgia. - : SAGE Publications. - 0333-1024 .- 1468-2982. ; 22:2, s. 112-116
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Tidskriftsartikel (refereegranskat)abstract
- In migraine and other primary headaches there is a strong vascular component. Besides the trigeminovascular components some of the associated symptoms point to the involvement of brain stem regions. The central limb of the trigeminal vascular pathway is its projection to the trigeminal nucleus caudalis (TNC) and to the C1-C2 levels of the spinal cord. The aim of the present study was to demonstrate the occurrence of some neurotransmitters in these regions in man. In both the TNC and in the Rexed's laminae I and II of the dorsal horns at the C1 and C2 levels there were numerous substance P immunoreactive fibres. Fibres containing calcitonin gene-related peptide (CGRP) and pituitary adenylate cyclase-activating peptide (PACAP) were moderately dense in number. Fibres containing vasoactive intestinal peptide (VIP) or nitric oxide synthase (NOS) were not seen in the TNC or at the C1 and C2 levels of the spinal cord.
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| 47. |
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| 48. |
- Uddman, Rolf, et al.
(författare)
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Neurotransmitter candidates in the vomeronasal organ of the rat.
- 2007
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Ingår i: Acta Oto-Laryngologica. - : Informa UK Limited. - 1651-2251 .- 0001-6489. ; 127:9, s. 952-956
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Tidskriftsartikel (refereegranskat)abstract
- Conclusion: The rich supply of nerve fibres containing neurotransmitters, particularly those containing SP and CGRP, is suggested to be a prerequisite for the recognition of chemical irritants as part of a chemical sense. Objective: The present study was designed to examine the distribution of different neurotransmitter candidates in the vomeronasal organ (VNO) of rats. Materials and methods: The distribution of neurotransmitter candidates was studied in the vomeronasal organ of the rat using immunocytochemistry. Results: The neuronal marker protein gene product 9.5 revealed a very rich supply of nerve fibres within and beneath the sensory epithelium, around blood vessels and glands. A moderate supply of nerve fibres containing tyrosine hydroxylase and neuropeptide Y was mostly seen close to blood vessels. Numerous nerve fibres containing nitric oxide synthase and vasoactive intestinal peptide were seen around blood vessels and in the subepithelial layer, with occasional fibres within the epithelium. Only few fibres located in the subepithelial layer contained pituitary adenylate cyclase activating peptide. Nerve fibres containing substance P and in particular calcitonin gene-related peptide were abundant in and beneath the epithelium and scattered in the submucosal layers around blood vessels.
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| 49. |
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