ENDOTHELIN-1 POTENTIATES SMOKE-INDUCED ACUTE LUNG INFLAMMATION
ENDOTHELIN-1 POTENTIATES SMOKE-INDUCED ACUTE LUNG INFLAMMATION
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DOI：
10.1080/01902140802389701
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发表时间：
2008-01-01
影响因子：
1.7
通讯作者：
Cantor, Jerome O.
中科院分区：
文献类型：
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作者：
Bhavsar, Tapan M.;Liu, Xingjian;Cantor, Jerome O.
本研究探讨了内皮素-1（ET-1）在短期香烟烟雾暴露诱导的急性肺部炎症中的作用。仓鼠接受腹腔注射ET-1，然后连续3天暴露于烟雾中2小时。然后使用以下参数评价肺的炎症变化：（1）肺组织病理学，（2）支气管肺泡灌洗液（BALF）的中性粒细胞含量，（3）肿瘤坏死因子受体1（TNFR 1）标记的BALF巨噬细胞百分比，和（4）肺泡间隔细胞凋亡。结果表明，ET- 1显着放大烟雾对这些炎症标志物的影响，这些反应可以通过预处理与一种新的内皮素受体A拮抗剂，HJP 272阻断。特别是，外源性ET-1诱导BALF中性粒细胞显著增加，这与该介质作为炎症细胞“看门人”的作用一致。"
The current study examined the role of endothelin-1 (ET-1) in mediating acute lung inflammation induced by short-term cigarette smoke exposure. Hamsters received intraperitoneal injections of ET-1, followed by a 2-hour period of smoke exposure, for 3 consecutive days. The lungs were then evaluated for inflammatory changes, using the following parameters: (1) lung histopathology, (2) neutrophil content of bronchoalveolar lavage fluid (BALF), (3) percent tumor necrosis factor receptor 1 (TNFR1)-labeled BALF macrophages, and (4) alveolar septal cell apoptosis. Results indicate that ET- 1 significantly amplified the effect of smoke on each of these inflammatory markers and that these responses could be blocked by pretreatment with a novel endothelin receptor A antagonist, HJP272. In particular, exogenous ET-1 induced a marked increase in BALF neutrophils, consistent with a role for this mediator as an inflammatory cell "gatekeeper."