Early production of IL-17 protects against acute pulmonary Pseudomonas aeruginosa infection in mice
Early production of IL-17 protects against acute pulmonary Pseudomonas aeruginosa infection in mice
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DOI：
10.1111/j.1574-695x.2010.00764.x
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发表时间：
2011-03-01
影响因子：
--
通讯作者：
Wan, Huanying
中科院分区：
文献类型：
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作者：
Liu, Jialin;Feng, Yun;Wan, Huanying
白细胞介素-17（IL-17）参与针对细胞外细菌的保护。然而，IL-17可能对慢性肺铜绿假单胞菌感染的宿主有害。IL-17在急性肺部铜绿假单胞菌感染中的作用仍不清楚。在此，我们评估了IL-17在急性肺铜绿假单胞菌感染中的作用以及白细胞介素的来源。急性铜绿假单胞菌感染小鼠后，IL-17的产生迅速增加。我们随后检查了IL-17在急性感染中的作用，发现感染16小时后，与IgG（2a）治疗的小鼠相比，IL-17中和抗体治疗的小鼠支气管肺泡灌洗液中的细菌多100倍。抗IL-17处理的小鼠中的主要浸润细胞是淋巴细胞而不是嗜中性粒细胞。同时，在抗IL-17治疗的小鼠中观察到更多的肺组织损伤和病理学变化。Th 17细胞是IL-17的来源之一。结论：小鼠急性肺部铜绿假单胞菌感染时，IL-17的早期产生对肺组织具有保护作用，Th 17细胞是急性肺部铜绿假单胞菌感染时IL-17的来源之一。总之，IL-17和Th 17细胞有助于体内急性肺铜绿假单胞菌感染的发病机制。
Interleukin-17 (IL-17) is involved in protection against extracellular bacteria. However, IL-17 is likely to be deleterious to a host with chronic pulmonary Pseudomonas aeruginosa infection. The role of IL-17 during acute pulmonary P. aeruginosa infection remains unknown. Here, we evaluated the role that IL-17 plays in acute pulmonary P. aeruginosa infection and the source of the interleukin. The production of IL-17 increased rapidly after acute pulmonary P. aeruginosa infection in mice. We subsequently examined the role of IL-17 in acute infection and found 100 times more bacteria in the bronchoalveolar lavage fluid of mice treated with an IL-17-neutralizing antibody compared with the IgG(2a)-treated mice after 16 h of infection. The main infiltrating cells in the anti-IL-17-treated mice were lymphocytes rather than neutrophils. Consistently, more tissue damage and pathological changes in the lung were observed in the anti-IL-17-treated mice. We also found that Th17 cells are one of the sources of IL-17. We conclude that the early production of IL-17 plays a protective role during acute pulmonary P. aeruginosa infection in mice and that Th17 cells are one of the sources of IL-17 during acute pulmonary P. aeruginosa infection. Altogether, IL-17 and Th17 cells contribute to the pathogenesis of acute pulmonary P. aeruginosa infection in vivo.