{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,29]],"date-time":"2026-07-29T20:59:09Z","timestamp":1785358749790,"version":"3.55.0"},"reference-count":56,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2004,5,12]],"date-time":"2004-05-12T00:00:00Z","timestamp":1084320000000},"content-version":"vor","delay-in-days":11,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Clin Experimental Allergy"],"published-print":{"date-parts":[[2004,5]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p><jats:bold>Background\n\t\t\t\t\t<\/jats:bold> Epidemiological evidence suggests that infection with <jats:italic>Mycobacterium tuberculosis<\/jats:italic> protects children against asthma. Several laboratories have shown that, in mouse models of allergic inflammation, administration of the whole live tuberculosis vaccine, <jats:italic>Mycobacterium bovis<\/jats:italic> bacillus Calmette\u2013Guerin (BCG), prevents ovalbumin (OVA)\u2010induced pulmonary eosinophilia.<\/jats:p><jats:p><jats:bold>Objective\n\t\t\t\t\t<\/jats:bold> The aim of this study was to characterize specific <jats:italic>M. tuberculosis<\/jats:italic> molecules that are known to modulate immune responses to see if they affected pulmonary eosinophilia and bronchial hyper\u2010responsiveness.<\/jats:p><jats:p><jats:bold>Methods\n\t\t\t\t\t<\/jats:bold> C57Bl\/6 mice were sensitized to OVA on days 0 and 7 and subsequently challenged with OVA on day 14 over a 3\u2010day period. Pulmonary eosinophilia and bronchial hyper\u2010responsiveness were measured 24\u2003h following the last antigen challenge. In some groups, mice were pre\u2010treated with <jats:italic>M. tuberculosis<\/jats:italic> or <jats:italic>M. tuberculosis<\/jats:italic> chaperonins (Cpns)60.1, 60.2 and 10, and the effect of this treatment on the allergic inflammatory response to aerosolized OVA was established.<\/jats:p><jats:p><jats:bold>Results\n\t\t\t\t\t<\/jats:bold> We show that <jats:italic>M. tuberculosis<\/jats:italic> Cpns inhibit allergen\u2010induced pulmonary eosinophilia in the mouse. Of the three Cpns produced by <jats:italic>M. tuberculosis<\/jats:italic>, Cpn60.1, Cpn10 and Cpn60.2, the first two are effective in preventing eosinophilia when administered by the intra\u2010tracheal route. Furthermore, the increase in airways sensitivity to inhaled methacholine following OVA challenge of immunized mice was suppressed following treatment with Cpn60.1. The allergic inflammatory response was also characterized by an increase in Th2 cytokines IL\u20104 and IL\u20105 in bronchoalveolar lavage fluid, which was also suppressed following treatment with Cpn60.1.<\/jats:p><jats:p><jats:bold>Conclusion\n\t\t\t\t\t<\/jats:bold> These data show that bacterial Cpns can suppress eosinophil recruitment and bronchial hyper\u2010responsiveness in a murine model of allergic inflammation.<\/jats:p>","DOI":"10.1111\/j.1365-2222.2004.1931.x","type":"journal-article","created":{"date-parts":[[2004,5,12]],"date-time":"2004-05-12T15:26:32Z","timestamp":1084375592000},"page":"712-719","source":"Crossref","is-referenced-by-count":52,"title":["Effect of <i>Mycobacterium tuberculosis<\/i> chaperonins on bronchial eosinophilia and hyper\u2010responsiveness in a murine model of allergic 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