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This view is based on observations<jats:italic>in vitro<\/jats:italic>and in airway lumen with unknown translatability to airway tissues<jats:italic>in vivo<\/jats:italic>. In fact, apoptotic eosinophils have not been detected in human diseased airway tissues whereas cytolytic eosinophils abound and constitute a major mode of degranulation of these cells. Also, Fas receptor stimulation may bypass the apoptotic pathway and directly evoke cytolysis of non-apoptotic cells. We thus hypothesized that effects of anti-Fas mAb<jats:italic>in vivo<\/jats:italic>may include both apoptosis and cytolysis of eosinophils and, hence, that established eosinophilic inflammation may not resolve by this treatment.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Weeklong daily allergen challenges of sensitized mice were followed by airway administration of anti-Fas mAb. BAL was performed and airway-pulmonary tissues were examined using light and electron microscopy. Lung tissue analysis for CC-chemokines, apoptosis, mucus production and plasma exudation (fibrinogen) were performed.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Anti-Fas mAb evoked apoptosis of 28% and cytolysis of 4% of eosinophils present in allergen-challenged airway tissues. Furthermore, a majority of the apoptotic eosinophils remained unengulfed and eventually exhibited secondary necrosis. A striking histopathology far beyond the allergic inflammation developed and included degranulated eosinophils, neutrophilia, epithelial derangement, plasma exudation, mucus-plasma plugs, and inducement of 6 CC-chemokines. In animals without eosinophilia anti-Fas evoked no inflammatory response.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>An efficient inducer of eosinophil apoptosis in airway tissues<jats:italic>in vivo<\/jats:italic>, anti-Fas mAb evoked unprecedented asthma-like inflammation in mouse allergic airways. This outcome may partly reflect the ability of anti-Fas to evoke direct cytolysis of non-apoptotic eosinophils in airway tissues. Additionally, since most apoptotic tissue eosinophils progressed into the pro-inflammatory cellular fate of secondary necrosis this may also explain the aggravated inflammation. Our data indicate that Fas receptor mediated eosinophil apoptosis in airway tissues<jats:italic>in vivo<\/jats:italic>may cause severe disease exacerbation due to direct cytolysis and secondary necrosis of eosinophils.<\/jats:p><\/jats:sec>","DOI":"10.1186\/1465-9921-6-90","type":"journal-article","created":{"date-parts":[[2005,8,9]],"date-time":"2005-08-09T18:14:00Z","timestamp":1123611240000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":28,"title":["Anti-Fas mAb-induced apoptosis and cytolysis of airway tissue eosinophils aggravates rather than resolves established inflammation"],"prefix":"10.1186","volume":"6","author":[{"given":"Lena","family":"Uller","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kristina","family":"Rydell-T\u00f6rm\u00e4nen","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Carl GA","family":"Persson","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jonas S","family":"Erjef\u00e4lt","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2005,8,8]]},"reference":[{"issue":"7","key":"328_CR1_328","doi-asserted-by":"publisher","first-page":"957","DOI":"10.1172\/JCI200114122","volume":"108","author":"VA Fadok","year":"2001","unstructured":"Fadok VA, Bratton DL, Henson PM: Phagocyte receptors for apoptotic cells: recognition, uptake, and consequences. 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