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- Benson, Mikael, 1954
(författare)
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Pathophysiological effects of glucocorticoids on nasal polyps: an update.
- 2005
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Ingår i: Current opinion in allergy and clinical immunology. - : Lippincott Williams & Wilkins. - 1528-4050 .- 1473-6322. ; 5:1, s. 31-5
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Forskningsöversikt (refereegranskat)abstract
- PURPOSE OF REVIEW: The exact mechanisms by which glucocorticoids exert their beneficial effects on nasal polyps are not clearly defined. Nasal polyps, asthma and allergic rhinitis share common features such as mucosal infiltration with eosinophils and mast cells as well as local IgE production. The present review is an update on the pathophysiological mechanisms of glucocorticoids on nasal polyps described during the last 2 years. RECENT FINDINGS: The reduction of leukocyte numbers in nasal polyps following glucocorticoid treatment depends on several mechanisms, for example altered balance between the two isoforms of the human glucocorticoid receptors, GRalpha and GRbeta. Another explanation may be inhibition of CD4+ T by CD8+ T cells. Increased expression of the antiinflammatory cytokine transforming growth factor beta may contribute to this. A DNA microarray study which examined the expression of some 22 000 genes showed increased expression of several antiinflammatory genes in nasal polyps after treatment with glucocorticoids. The antiinflammatory gene that increased most was uteroglobin (also known as Clara cell protein 16) which is abundantly expressed in airway secretions and thought to have an important role in regulating inflammation. SUMMARY: Glucocorticoids affect both pro and antiinflammatory pathways in nasal polyps. Upregulation of antiinflammatory genes such as transforming growth factor beta and uteroglobin may play an important role. Elucidation of these mechanisms may help us to understand not only the effects of glucocorticoids on nasal polyps, but also on related disorders such as allergic rhinitis and asthma.
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| 2. |
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| 3. |
- Björkstén, Bengt
(författare)
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Primary prevention of atopic asthma.
- 2001
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Ingår i: Current Opinion in Allergy and Clinical Immunology. - : Ovid Technologies (Wolters Kluwer Health). - 1528-4050 .- 1473-6322. ; 1, s. 545-548
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Tidskriftsartikel (refereegranskat)
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| 4. |
- Björkstén, Bengt
(författare)
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The epidemiology of food allergy
- 2001
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Ingår i: Current Opinion in Allergy and Clinical Immunology. - : Ovid Technologies (Wolters Kluwer Health). - 1528-4050 .- 1473-6322. ; 1, s. 225-227
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Tidskriftsartikel (refereegranskat)
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| 5. |
- Bystrom, Jonas, et al.
(författare)
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Dissecting the role of eosinophil cationic protein in upper airway disease
- 2012
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Ingår i: Current Opinion in Allergy and Clinical Immunology. - 1528-4050 .- 1473-6322. ; 12:1, s. 18-23
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Forskningsöversikt (refereegranskat)abstract
- Purpose of review Eosinophil granulocyte myeloid cells are increased in atopic and nonatopic rhinitis, chronic rhinosinusitis (CRS) and atopic keratoconjunctivitis, diseases of the upper respiratory tract. Eosinophils contain several basic granule proteins, the best known being the eosinophil cationic protein (ECP). ECP is a cytotoxic, profibrotic ribonuclease, which is found deposited in these eosinophil-related diseases and is often used in parallel with blood eosinophilia to monitor those diseases. The contribution of eosinophils and their granule proteins to disease pathogenesis have been debated; recent findings might bring these cells to the center of attention. Recent findings Novel mediators of atopic disease, interleukin-17 (IL-17) and IL-33 have been found in the upper respiratory tract. These cytokines stimulate eosinophils to survival and degranulation, IL-17 via granulocyte-macrophage colony-stimulating factor (GM-CSF), and IL-33 directly. Transforming growth factor (TGF)-beta has been found in CRS and atopic keratoconjunctivitis mucosa, its production possibly stimulated by ECP. ECP is detected in nasal mucosa of local allergic reactions, entopy, in rhinitis and CRS. ECP might be released from freely circulating eosinophil granules or in association with eosinophil mitochondrial DNA, both means of release for pathogen defence. Summary Novel evidence suggests that eosinophils and ECP might have new prominent roles in development of diseases of the upper respiratory tract.
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| 7. |
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| 8. |
- Marklund, Birgitta, et al.
(författare)
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Food hypersensitivity and quality of life
- 2007
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Ingår i: Current Opinion in Allergy and Clinical Immunology. - 1528-4050 .- 1473-6322. ; 7, s. 279-287
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Forskningsöversikt (övrigt vetenskapligt/konstnärligt)
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| 9. |
- Millqvist, Eva, 1949
(författare)
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Mechanisms of increased airway sensitivity to occupational chemicals and odors.
- 2008
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Ingår i: Current opinion in allergy and clinical immunology. - 1528-4050. ; 8:2, s. 135-9
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Tidskriftsartikel (refereegranskat)abstract
- PURPOSE OF REVIEW: Airway symptoms induced by chemicals and odors are common problems that are also reported after contact with substances normally regarded as nontoxic. This article reviews current findings and opinions regarding mechanisms of increased airway sensitivity to occupational chemicals and odors. RECENT FINDINGS: Individuals exposed to organic solvents during work had more nasal irritation and lower threshold to pyridine odor compared with a nonexposed control group. Six percentage of a general population in Sweden had pronounced airway chemical sensitivity and augmented capsaicin cough sensitivity, known to reflect the sensory nerve reactivity of the airways. The cough sensitivity was associated with changed levels of nerve growth factor in nasal lavage and such patients had longstanding symptoms influencing their working capacity. Positron emission tomography activation studies with several different odorants showed in patients with odor-associated symptoms an odorant-related increase in activation of the anterior cingulate cortex and cuneus-precuneus in comparison with a control group. SUMMARY: In subgroups of individuals with airway symptoms induced by chemicals and odors, there seems to be a sustainable physiological mechanism behind the reactions. An increased vulnerability to stress cannot be neglected as a confounding factor in some sensitive individuals.
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| 10. |
- Mogensen, Ida, et al.
(författare)
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Systemic and breath biomarkers for asthma : an update
- 2020
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Ingår i: Current Opinion in Allergy and Clinical Immunology. - 1528-4050 .- 1473-6322. ; 20:1, s. 71-79
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Forskningsöversikt (refereegranskat)abstract
- PURPOSE OF REVIEW: Finding suitable biomarkers to phenotype asthma, identify individuals at risk of worsening and guide treatment is highly prioritized in asthma research. We aimed to provide an analysis of currently used and upcoming biomarkers, focusing on developments published in the past 2 years.RECENT FINDINGS: Type 2 inflammation is the most studied asthma mechanism with the most biomarkers in the pipeline. Blood eosinophils and fractional exhaled nitric oxide (FeNO) are those most used clinically. Recent developments include their ability to identify individuals at higher risk of exacerbations, faster decline in lung function and more likely to benefit from anti-IL-5 and anti-IL-4/-13 treatment. Certain patterns of urinary eicosanoid excretion also relate to type 2 inflammation. Results of recent trials investigating the use of serum periostin or dipeptidyl peptidase-4 to guide anti-IL-13 therapy were somewhat disappointing. Less is known about non-type 2 inflammation but blood neutrophils and YKL-40 may be higher in patients with evidence of non-type 2 asthma. Volatile organic compounds show promise in their ability to distinguish both eosinophilic and neutrophilic asthma.SUMMARY: The ultimate panel of biomarkers for identification of activated inflammatory pathways and treatment strategies in asthma patients still lies in the future, particularly for non-type 2 asthma, but potential candidates are available.
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