Interleukin-17 and lung host defense against Klebsiella pneumoniae infection
Interleukin-17 and lung host defense against Klebsiella pneumoniae infection
复制标题
白细胞介素 - 17与肺部针对肺炎克雷伯菌感染的宿主防御
DOI：
10.1165/ajrcmb.25.3.4424
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发表时间：
2001-09-01
影响因子：
6.4
通讯作者：
Kolls, JK
中科院分区：
文献类型：
--
作者：
Ye, P;Garvey, PB;Kolls, JK
细菌性肺炎仍然是世界范围内发病率和死亡率的重要原因，特别是在免疫缺陷患者中。细胞因子和趋化因子是响应入侵病原体而表达的关键分子，并且是正常肺细菌宿主防御所必需的。在这里，我们表明，白细胞介素（IL）-17，主要由CD 4 + T细胞产生的一种新的细胞因子，在肺炎克雷伯氏菌的挑战后，在肺中产生一个区室化的方式。此外，使用编码鼠IL-17的重组腺病毒（AdIL-17）在肺隔室中过表达IL-17导致肿瘤坏死因子-α、IL-1 β、巨噬细胞炎性蛋白-2和粒细胞集落刺激因子（G-CSF）的局部诱导;增强多形核白细胞募集，并增强细菌清除和用K.肺炎。然而，同时用AdIL-17治疗在鼻内K.肺炎攻毒。这些数据表明，IL-17可能在引发增强的趋化因子和G-CSF的生产在肺部感染的情况下，最佳时机的基因治疗与IL-17可以增强宿主防御细菌性肺炎的作用。
Bacterial pneumonia remains an important cause of morbidity and mortality worldwide, especially in immune-com promised patients. Cytokines and chemokines are critical molecules expressed in response to invading pathogens and are necessary for normal lung bacterial host defenses. Here we show that interleukin (IL)-17, a novel cytokine produced largely by CD4+ T cells, is produced in a compartmentalized fashion in the lung after challenge with Klebsiella pneumoniae. Moreover, overexpression of IL-17 in the pulmonary compartment using a recombinant adenovirus encoding murine IL-17 (AdlL-17) resulted in the local induction of tumor necrosis factor-alpha, IL-1 beta, macrophage inflammatory protein-2, and granulocyte colony-stimulating factor (G-CSF); augmented polymorphonuclear leukocyte recruitment, and enhanced bacterial clearance and survival after challenge with K. pneumoniae. However, simultaneous treatment with AdIL-17 provided no survival benefit after intranasal K. pneumoniae challenge. These data show that IL-17 may have a role in priming for enhanced chemokine and G-CSF production in the context of lung infection and that optimally timed gene therapy with IL-17 may augment host defense against bacterial pneumonia.