| 1. |
- Bogefors, Jesper, et al.
(författare)
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LEAP-2, LL-37 and RNase7 in tonsillar tissue: downregulated expression in seasonal allergic rhinitis.
- 2014
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Ingår i: Pathogens and Disease. - 2049-632X. ; 72:1, s. 55-60
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Tidskriftsartikel (refereegranskat)abstract
- In the upper airway, the production of antimicrobial peptides (AMPs) protects against bacteria, viruses and fungi. Previous investigations have revealed downregulated expression of AMPs in different manifestations of allergic disease. In this study, we examined the expression of LL-37, RNase7 and LEAP-2 in tonsillar tissue and studied a possible relation to seasonal allergic rhinitis (SAR).
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| 2. |
- Bogefors, Jesper, et al.
(författare)
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Reduced tonsillar expression of human β-defensin 1, 2 and 3 in allergic rhinitis.
- 2012
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Ingår i: FEMS Immunology and Medical Microbiology. - 1574-695X. ; 65:3, s. 431-438
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Tidskriftsartikel (refereegranskat)abstract
- Airway infections are known to cause exacerbations of allergy and asthma. Tonsils constitute a primary site for microbial recognition and triggering of the immune system in the airways. Human β-defensins (HBDs) are antimicrobial peptides with an important role in this defense. Our aim was to investigate HBD1-3 in tonsillar tissue and their potential role in allergic rhinitis (AR). Tonsils, obtained from patients with AR and non-allergic controls, and isolated tonsillar CD4(+) , CD8(+) and CD19(+) lymphocytes were analyzed for HBD1-3 expression using real-time RT-PCR and/or immunohistochemistry. Tonsillar tissue, mixed tonsillar lymphocytes and airway epithelial cells (AECs) were cultured with or without IL-4, IL-5, IL-13 or histamine followed by measurements of HBD1-3 release using ELISA. HBD1-3 were present in tonsillar tissue, including epithelial, CD4(+) , CD8(+) and CD19(+) cells. The expression was reduced in allergic compared to healthy tonsils. Stimulation of AECs with IL-4, IL-5 and histamine down-regulated the HBD release, whereas no effects were seen in cultured tonsils or lymphocytes. This study demonstrates presence of HBD1-3 in tonsils and that the levels are reduced in patients with AR. Together with the down-regulation of HBDs in epithelial cells in the presence of allergic mediators suggest that AR patients have an impaired antimicrobial defense that might make them more susceptible to respiratory tract infections. © 2012 Federation of European Microbiological Societies. Published by Blackwell Publishing Ltd. All rights reserved.
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| 3. |
- 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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| 4. |
- Bogefors, Jesper, et al.
(författare)
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Upregulated levels of human β-defensins in patients with seasonal allergic rhinitis after allergen-specific immunotherapy treatment.
- 2013
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Ingår i: International Forum of Allergy & Rhinology. - : Wiley. - 2042-6984 .- 2042-6976. ; 3:2, s. 99-103
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Antimicrobial peptides (AMPs) are important actors in the innate immune system. One class of AMPs is the human β-defensins (HBDs), a group of small peptides with a broad spectrum of antimicrobial activities. Expression of HBDs is downregulated in different manifestations of allergic disease. In this study, we examine whether allergen-specific immunotherapy (ASIT) affects the nasal levels of HBDs in patients with seasonal allergic rhinitis (SAR). METHODS: Nasal biopsies were examined for the occurrence of HBD1-3 with real-time reverse-transcription polymerase chain reaction (RT-PCR) and immunohistochemistry. Nasal lavage (NAL) fluids from healthy individuals, untreated SAR patients and SAR patients before and after ASIT were analyzed for levels of HBD1-3 using enzyme-linked immunosorbent assay (ELISA). RESULTS: Examination of nasal biopsies revealed HBD1-3 expression at gene level as well as at protein level in all samples tested. HBD1 and HBD3 messenger RNA (mRNA) levels were downregulated in SAR patients compared to healthy individuals. All HBDs were found in NAL fluids. SAR patients having completed 3 years of ASIT displayed higher levels of HBD1 and HBD2 than before treatment, whereas levels of HBD3 were unaffected. CONCLUSION: The present study demonstrates an upregulation of HBD1 and HBD2 in SAR patients after completion of ASIT. This may reflect the importance of an intact innate immune response as part of our defense against infections among allergic individuals.
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