{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,21]],"date-time":"2026-03-21T20:16:00Z","timestamp":1774124160274,"version":"3.50.1"},"reference-count":29,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2006,11,13]],"date-time":"2006-11-13T00:00:00Z","timestamp":1163376000000},"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":[[2006,12]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p><jats:bold>Background\n\t\t\t\t\t<\/jats:bold> IL\u201025, a novel member of the IL\u201017 cytokine family, promotes CD4<jats:sup>+<\/jats:sup> T\u2010helper 2 lymphocyte\u2010like (Th type\u20102) inflammatory responses in the lung. Although IL\u201025 up\u2010regulates IL\u201013 in the lung, the contribution of this and other type 2 cytokine signalling pathways to the induction and persistence of airways hyper\u2010reactivity (AHR) and allergic inflammation are unclear.<\/jats:p><jats:p><jats:bold>Objective\n\t\t\t\t\t<\/jats:bold> To determine the downstream factors employed by IL\u201025 to induce Th type\u20102 pulmonary inflammation and AHR.<\/jats:p><jats:p><jats:bold>Methods\n\t\t\t\t\t<\/jats:bold> IL\u201025 was delivered to the airways of BALB\/c mice by intra\u2010tracheal (i.t.) instillation and AHR and Th type\u20102 inflammatory responses were characterized in wild type (WT) and Th type\u20102\u2010cytokine and \u2010signalling pathway\u2010deficient (\u2212\/\u2212) mice.<\/jats:p><jats:p><jats:bold>Results\n\t\t\t\t\t<\/jats:bold> IL\u201025 treatment resulted in AHR, eosinophilic inflammation, mucus hypersecretion and a progressive increase in the production of Th type\u20102 cytokines in the lungs. Levels of arginase\u2010I (arg\u2010I) and eotaxin were also elevated by IL\u201025 treatment. A significant reduction in AHR, and attenuation of mucus production was observed in IL\u201025\u2010treated IL\u201013<jats:sup>\u2212\/\u2212<\/jats:sup>, IL\u20104 receptor alpha (IL\u20104R\u03b1<jats:sup>\u2212\/\u2212<\/jats:sup>)\u2010 and signal\u2010transducer\u2010and\u2010activator\u2010of\u2010transcription\u2010factor\u20106 (STAT6<jats:sup>\u2212\/\u2212<\/jats:sup>)\u2010deficient mice. AHR was also inhibited in IL\u20104<jats:sup>\u2212\/\u2212<\/jats:sup>\u2010 and IL\u20105\/eotaxin(1)<jats:sup>\u2212\/\u2212<\/jats:sup>\u2010 deficient mice treated with IL\u201025, however, mucus hypersecretion was not completely ablated. IL\u201025 promoted Th type\u20102 responses by directly acting on na\u00efve T cells.<\/jats:p><jats:p><jats:bold>Conclusion\n\t\t\t\t\t<\/jats:bold> IL\u201025 potently (single dose) induces sustained AHR and acute pulmonary inflammation with eosinophilia. IL\u201025\u2010induced AHR is dependent on the production of Th type\u20102 cytokines, and removal of IL\u201013 and its signal transduction pathway prevents IL\u201025\u2010induced airways inflammation and AHR. IL\u201025 potently induces inflammatory cascades that may exacerbate allergic airways inflammation by promoting Th type\u20102 cytokine responses in conjunction with the up\u2010regulation of factors (eotaxin and arg\u2010I) that can amplify inflammation associated with allergic disorders. Dysregulation in IL\u201025 production may predispose to features of allergic airways disease.<\/jats:p>","DOI":"10.1111\/j.1365-2222.2006.02595.x","type":"journal-article","created":{"date-parts":[[2006,11,13]],"date-time":"2006-11-13T17:38:16Z","timestamp":1163439496000},"page":"1575-1583","source":"Crossref","is-referenced-by-count":80,"title":["Mechanism of interleukin\u201025 (IL\u201017E)\u2010induced pulmonary inflammation and airways hyper\u2010reactivity"],"prefix":"10.1111","volume":"36","author":[{"given":"T.","family":"Sharkhuu","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"K. 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