Autoinducer-2 promotes Pseudomonas aeruginosa PAO1 acute lung infection via the IL-17A pathway

作者全名："Li, Hongdong; Li, Xingyuan; Ai, Qing; Tan, Liping"

作者地址："[Li, Hongdong; Ai, Qing; Tan, Liping] Chongqing Med Univ, Dept Emergency, Childrens Hosp, Chongqing, Peoples R China; [Li, Hongdong; Ai, Qing; Tan, Liping] Minist Educ, Key Lab Child Dev & Disorders, Chongqing, Peoples R China; [Li, Hongdong; Ai, Qing; Tan, Liping] Natl Clin Res Ctr Child Hlth & Disorders, Chongqing, Peoples R China; [Li, Hongdong; Ai, Qing; Tan, Liping] China Int Sci & Technol Cooperat Base Child Dev &, Chongqing, Peoples R China; [Li, Hongdong; Ai, Qing; Tan, Liping] Chongqing Key Lab Child Infect & Immun, Chongqing, Peoples R China; [Li, Xingyuan] Chongqing Red Cross Hosp, Dept Pharm, Chongqing, Peoples R China"

通信作者："Tan, LP (通讯作者)，Chongqing Med Univ, Dept Emergency, Childrens Hosp, Chongqing, Peoples R China.; Tan, LP (通讯作者)，Minist Educ, Key Lab Child Dev & Disorders, Chongqing, Peoples R China.; Tan, LP (通讯作者)，Natl Clin Res Ctr Child Hlth & Disorders, Chongqing, Peoples R China.; Tan, LP (通讯作者)，China Int Sci & Technol Cooperat Base Child Dev &, Chongqing, Peoples R China.; Tan, LP (通讯作者)，Chongqing Key Lab Child Infect & Immun, Chongqing, Peoples R China."

来源：FRONTIERS IN MICROBIOLOGY

ESI学科分类：MICROBIOLOGY

WOS号：WOS:000844357400001

JCR分区：Q2

影响因子：5.2

年份：2022

卷号：13

期号：　

开始页：　

结束页：　

文献类型：Article

关键词：Pseudomonas aeruginosa; autoinducer-2; Th17 cell; interleukin-17A; infection

摘要："Pseudomonas aeruginosa is an opportunistic pathogenic bacterium that causes various acute and chronic lung infections in immunocompromised patients. We previously found that a quorum sensing (QS) signal, namely, autoinducer-2 (AI-2), facilitates the pathogenicity of the wild-type (WT) P. aeruginosa PAO1 strain in vitro and in vivo. However, the immunological mechanism that leads to pulmonary injury remains to be elucidated. In this study, we aimed to investigate the effects of AI-2 on interleukin-17A (IL-17A) production during acute P. aeruginosa PAO1 lung infection using a mouse model, with an emphasis on the underlying immunological mechanism. Compared to infection with P. aeruginosa PAO1 alone, infection with P. aeruginosa PAO1 combined with AI-2 treatment resulted in significantly increased levels of IL-17A, numbers of Th17 cells and levels of STAT3 in the lung tissues of WT mice (P < 0.05), as well as more serious lung damage. In contrast, the concentrations of the proinflammatory cytokines IL-1 alpha, IL-1 beta, and IL-6 and the chemokine keratinocyte-derived chemokine (KC) were significantly reduced during P. aeruginosa lung infection in IL-17A(-/-) mice compared with WT mice (P < 0.05), and no effects were observed after AI-2 treatment (P > 0.05). Furthermore, the level of IL-17A in the lungs of WT mice was significantly reduced following infection with a P. aeruginosa strain harboring mutations in the QS genes lasR and rhlR compared with the level of IL-17A following infection with P. aeruginosa PAO1. Our data suggest that AI-2 promotes P. aeruginosa PAO1 acute lung infection via the IL-17A pathway by interfering with the QS systems of P. aeruginosa. IL-17A may be a therapeutic target for the treatment of acute P. aeruginosa lung infections in the clinic."

基金机构：　

基金资助正文：