{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T10:52:56Z","timestamp":1791024776837,"version":"4.1.0"},"reference-count":46,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2011,7,4]],"date-time":"2011-07-04T00:00:00Z","timestamp":1309737600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Clin Experimental Allergy"],"published-print":{"date-parts":[[2011,10]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p>\n            <jats:bold>Background <\/jats:bold> Interleukin (IL)\u201025 (IL\u201017E) is a potent inducer of the type\u20102 immune effector response. Previously we have demonstrated that a neutralizing anti\u2010IL\u201025 antibody, given during the establishment of ovalbumin\u2010specific lung allergy, abrogates airways hyperreactivity.<\/jats:p><jats:p>\n            <jats:bold>Objective <\/jats:bold> Blocking IL\u201025 results in the suppression of IL\u201013, a cytokine known to exacerbate pulmonary inflammation, and an unexpected reciprocal increase in IL\u201017A. The role of IL\u201017A in asthma is complex with reports of both pro\u2010inflammatory and anti\u2010inflammatory functions. Our aim was to determine the influence of IL\u201017A in regulating IL\u201025\u2010dependent lung allergy.<\/jats:p><jats:p>\n            <jats:bold>Method <\/jats:bold> Neutralizing antibodies to IL\u201025 and\/or IL\u201017A 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.<\/jats:p><jats:p>\n            <jats:bold>Results <\/jats:bold> Neutralization of IL\u201025 correlated with a decrease in IL\u201013 levels and an increase in IL\u201017A production, and an accompanying prevention of airway hyperresponsiveness (AHR). Notably, the blocking of IL\u201017A reversed the protective effects of treating with anti\u2010IL\u201025 antibodies, resulting in the re\u2010expression of several facets of the lung inflammatory response, including IL\u201013 and eotaxin production, eosinophilia and AHR. Using mice over\u2010expressing IL\u201013 we demonstrate that treatment of these mice with anti\u2010IL\u201025 fails to suppress IL\u201013 levels and in turn IL\u201017A levels remain suppressed.<\/jats:p><jats:p>\n            <jats:bold>Conclusions and Clinical Relevance <\/jats:bold> IL\u201013 is known to be an important inducer of lung inflammation, causing goblet cell hyperplasia and promoting airways hyperreactivity. Our data now demonstrate that IL\u201013 also plays an important role in the genesis of lung inflammation downstream of IL\u201025 by suppressing a protective IL\u201017A response. These findings also highlight the important reciprocal interplay of the IL\u201017 family members, IL\u201025 and IL\u201017A, in regulating allergic lung responses and suggest that the balance of IL\u201017A, together with IL\u201025, will be an important consideration in the treatment of allergic asthma.<\/jats:p><jats:p>\n            <jats:italic>Cite this as<\/jats:italic>: J. L. Barlow, R. J. Flynn, S. J. Ballantyne and A. N. J. McKenzie, <jats:italic>Clinical &amp; Experimental Allergy<\/jats:italic>, 2011 (41) 1447\u20131455.<\/jats:p>","DOI":"10.1111\/j.1365-2222.2011.03806.x","type":"journal-article","created":{"date-parts":[[2011,7,4]],"date-time":"2011-07-04T16:16:51Z","timestamp":1309796211000},"page":"1447-1455","source":"Crossref","is-referenced-by-count":55,"title":["Reciprocal expression of IL\u201025 and IL\u201017A is important for allergic airways hyperreactivity"],"prefix":"10.1111","volume":"41","author":[{"given":"J. L.","family":"Barlow","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"R. J.","family":"Flynn","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S. J.","family":"Ballantyne","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A. N. 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