دورية أكاديمية
IL-9 protects against bleomycin-induced lung injury: involvement of prostaglandins.
| العنوان: | IL-9 protects against bleomycin-induced lung injury: involvement of prostaglandins. |
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| المؤلفون: | Arras, Mohammed, Louahed, Jamila, Heilier, Jean-François, Delos, Monique, Brombacher, Frank, Renauld, Jean-Christophe, Lison, Dominique, Huaux, François |
| المساهمون: | UCL - MD/MNOP - Département de morphologie normale et pathologique, UCL - MD/ESP - Ecole de santé publique, UCL - MD/MIGE - Département de microbiologie, d'immunologie et de génétique, UCL - (SLuc) Centre de toxicologie clinique, UCL - (SLuc) Service de biochimie médicale, UCL - (MGD) Service d'anatomie pathologique |
| المصدر: | The American Journal of Pathology : cellular and molecular biology of disease, Vol. 166, no. 1, p. 107-115 (2005) |
| بيانات النشر: | Elsevier Inc. |
| سنة النشر: | 2005 |
| المجموعة: | DIAL@USL-B (Université Saint-Louis, Bruxelles) |
| مصطلحات موضوعية: | Animals, Bleomycin, Bronchoalveolar Lavage Fluid, Indomethacin, Interleukin-9, L-Lactate Dehydrogenase, Lung, Lung Diseases, Lung Injury, Mice, Inbred Strains, Transgenic, Prostaglandins, Time Factors, Water Supply |
| الوصف: | IL-9 is a Th2 cytokine that exerts pleiotropic activities, and might be involved in the regulation of lung inflammatory processes. To characterize the activity of IL-9 on lung injury, we compared the pulmonary responses to bleomycin (blm) in IL-9 transgenic (Tg5) and wild-type (FVB) mice. Following intratracheal instillation of lethal doses of blm, the mortality rate was markedly reduced in Tg5 mice compared to their wild-type counterparts (ie, 25% mortality for Tg5 versus 85% for FVB mice, 21 days after instillation of 0.05U blm/mouse). Histological and biochemical analyses showed that blm induced less lung injury and less epithelial damage in Tg5 as compared to FVB animals. This protection of Tg5 mice was accompanied by an expansion of eosinophils and B cells in the lungs. In addition, TGF-beta and prostaglandin-E2 (PGE2) levels in broncho-alveolar lavage fluid were also increased in transgenic mice. The contribution of B cells and eosinophils to the protective mechanism did not appear essential since eosinophil-deficient (IL-5 KO) and B-deficient (muMT) mice overexpressing IL-9 were also resistant to high doses of blm. We could rule out that TGF-beta was a key factor in the protective effect of IL-9 by blocking this mediator with neutralizing antibodies. Indomethacin treatment, which inhibited PGE2 production in both strains, suppressed the protection in Tg5 mice, supporting the idea that IL-9 controls blm-induced lung injury through a prostaglandin-dependent mechanism. |
| نوع الوثيقة: | article in journal/newspaper |
| اللغة: | English |
| تدمد: | 0002-9440 1525-2191 |
| العلاقة: | boreal:25866; http://hdl.handle.net/2078.1/25866Test; info:pmid/15632004; urn:ISSN:0002-9440; urn:EISSN:1525-2191 |
| DOI: | 10.1016/S0002-9440(10)62236-5 |
| الإتاحة: | https://doi.org/10.1016/S0002-9440Test(10)62236-5 http://hdl.handle.net/2078.1/25866Test |
| حقوق: | info:eu-repo/semantics/openAccess |
| رقم الانضمام: | edsbas.6A069F8C |
| قاعدة البيانات: | BASE |
Full Text Finder | تدمد: | 00029440 15252191 |
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| DOI: | 10.1016/S0002-9440(10)62236-5 |