Cell signaling underlying the pathophysiology of pneumonia
Cell signaling underlying the pathophysiology of pneumonia
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DOI：
10.1152/ajplung.00138.2006
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发表时间：
2006-09-01
影响因子：
4.9
通讯作者：
Bhattacharya, Jahar
中科院分区：
文献类型：
--
作者：
Prince, Alice S.;Mizgerd, Joseph P.;Bhattacharya, Jahar
专题讨论会讨论了对肺炎发病的基本机制日益增长的兴趣。细菌利用肺的先天免疫机制，导致病理生理细胞信号传导。结果炎症发展，导致肺炎。已经确定了新的机制，气道中的细菌或细菌产物通过该机制诱导导致炎症后果的跨室信号传导。发言者讨论了转录因子NF-κ B B的激活，这是细菌与特定受体（如Toll样受体和TNF受体1（Prince））相互作用的结果，也是细胞因子诱导的结果（Mizgerd）。还考虑了临床环境中细菌毒力的机制（Wiener-Kronish）和肺泡-毛细血管信号传导机制在肺部炎症启动中的作用。
The symposium addressed the burgeoning interest in fundamental mechanisms underlying the onset of pneumonia. Bacteria exploit the lung's innate immune mechanism, resulting in pathophysiological cell signaling. As a consequence inflammation develops, leading to pneumonia. New mechanisms have been identified by which bacteria or bacterial products in the airway induce cross-compartmental signaling that leads to inflammatory consequences. The speakers addressed activation of the transcription factor, NF-kappa B occurring as a consequence of bacterial interactions with specific receptors, such as the Toll-like receptors and the TNF receptor 1 (Prince), or as a consequence of cytokine induction (Mizgerd). Also considered were mechanisms of bacterial virulence in the clinical setting (Wiener-Kronish) and the role of alveolar-capillary signaling mechanisms in the initiation of lung inflammation.