Liu Jialin, Feng Yun, Yang Kun, Li Qingyun, Ye Liang, Han Lizhong, Wan Huanying
Department of Pulmonary Medicine, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
FEMS Immunol Med Microbiol. 2011 Mar;61(2):179-88. doi: 10.1111/j.1574-695X.2010.00764.x. Epub 2011 Jan 18.
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.
白细胞介素-17(IL-17)参与抵御细胞外细菌。然而,IL-17可能对患有慢性铜绿假单胞菌肺部感染的宿主有害。IL-17在急性铜绿假单胞菌肺部感染中的作用尚不清楚。在此,我们评估了IL-17在急性铜绿假单胞菌肺部感染中所起的作用以及该白细胞介素的来源。小鼠急性铜绿假单胞菌肺部感染后,IL-17的产生迅速增加。我们随后研究了IL-17在急性感染中的作用,发现感染16小时后,用IL-17中和抗体处理的小鼠支气管肺泡灌洗液中的细菌数量比用IgG(2a)处理的小鼠多100倍。抗IL-17处理小鼠中的主要浸润细胞是淋巴细胞而非中性粒细胞。一致地,在抗IL-17处理的小鼠中观察到更多的肺组织损伤和病理变化。我们还发现Th17细胞是IL-17的来源之一。我们得出结论,IL-17的早期产生在小鼠急性铜绿假单胞菌肺部感染中起保护作用,并且Th17细胞是急性铜绿假单胞菌肺部感染期间IL-17的来源之一。总之,IL-17和Th17细胞在体内促成了急性铜绿假单胞菌肺部感染的发病机制。