NDLI: Reciprocal expression of IL-25 and IL-17A is important for allergic airways hyperreactivity.

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Reciprocal expression of IL-25 and IL-17A is important for allergic airways hyperreactivity.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Barlow, J. L. Flynn, R. J. Ballantyne, S. J. McKenzie, A. N. J.
Description	Country affiliation: United kingdom Author Affiliation: Barlow JL ( MRC Laboratory of Molecular Biology, Cambridge, UK. jbarlow@mrc-lmb.cam.ac.uk)
Abstract	BACKGROUND: Interleukin (IL)-25 (IL-17E) is a potent inducer of the type-2 immune effector response. Previously we have demonstrated that a neutralizing anti-IL-25 antibody, given during the establishment of ovalbumin-specific lung allergy, abrogates airways hyperreactivity. OBJECTIVE: Blocking IL-25 results in the suppression of IL-13, a cytokine known to exacerbate pulmonary inflammation, and an unexpected reciprocal increase in IL-17A. The role of IL-17A in asthma is complex with reports of both pro-inflammatory and anti-inflammatory functions. Our aim was to determine the influence of IL-17A in regulating IL-25-dependent lung allergy. METHOD: Neutralizing antibodies to IL-25 and/or IL-17A were administered during an experimental model of allergic asthma. Bronchoalveolar cell infiltrates and lung cytokine production were determined to assess lung inflammation. Invasive plethysmography was undertaken to measure lung function. RESULTS: Neutralization of IL-25 correlated with a decrease in IL-13 levels and an increase in IL-17A production, and an accompanying prevention of airway hyperresponsiveness (AHR). Notably, the blocking of IL-17A reversed the protective effects of treating with anti-IL-25 antibodies, resulting in the re-expression of several facets of the lung inflammatory response, including IL-13 and eotaxin production, eosinophilia and AHR. Using mice over-expressing IL-13 we demonstrate that treatment of these mice with anti-IL-25 fails to suppress IL-13 levels and in turn IL-17A levels remain suppressed. CONCLUSIONS AND CLINICAL RELEVANCE: IL-13 is known to be an important inducer of lung inflammation, causing goblet cell hyperplasia and promoting airways hyperreactivity. Our data now demonstrate that IL-13 also plays an important role in the genesis of lung inflammation downstream of IL-25 by suppressing a protective IL-17A response. These findings also highlight the important reciprocal interplay of the IL-17 family members, IL-25 and IL-17A, in regulating allergic lung responses and suggest that the balance of IL-17A, together with IL-25, will be an important consideration in the treatment of allergic asthma.
File Format	HTM / HTML
ISSN	09547894
Issue Number	10
Volume Number	41
e-ISSN	13652222
Journal	Clinical & Experimental Allergy
Language	English
Publisher	Wiley-Blackwell
Publisher Date	2011-10-01
Publisher Place	Great Britain (UK)
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Discipline Immunology Bronchial Hyperreactivity Immunology Interleukin-13 Metabolism Interleukin-17 Respiratory Hypersensitivity Animals Asthma Physiopathology Cytokines Biosynthesis Female Humans Lung Male Mice Mice, Inbred Balb C Mice, Knockout Ovalbumin Pneumonia Th2 Cells Journal Article Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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