Xu Xilin, Shao Bing, Wang Ran, Zhou Sijing, Tang Zhongzhi, Lu Weihua, Xiong Shengdao
Department of Emergency Medicine, Wuhan General Hospital of Guangzhou Military Command Wuhan 430070, China.
Tongji Medical College, Huazhong University of Science and Technology Wuhan 430030, China.
Int J Clin Exp Med. 2014 Apr 15;7(4):809-16. eCollection 2014.
Pseudomonas aeruginosa may cause severe or even fatal infection in hosts with immunodeficiency. Interleukin-17 (IL-17) is a newly discovered pro-inflammatory cytokine, which promotes the recruitment and activation of neutrophils in the respiratory tract by inducing release of chemokine C-X-C.
This study was conducted to explore the role of IL-17 in host defense against acute pseudomonas aeruginosa infection in lungs.
The expression of IL-17 and its downstream effectors (IL-1β, MIP-2 and G-CSF) were detected in mouse lungs with acute pseudomonas aeruginosa infection; 48 h after intratracheal administration of justice plasmid, mice were infected with pseudomonas aeruginosa again, and the bacterial clearance rate and the expression of downstream effectors of IL-17, as well as the mice death rate, were determined 6 h later.
The expression of IL-17 and its downstream effectors (IL-1β, MIP-2 and G-CSF) significantly increased in mouse lungs with acute pseudomonas aeruginosa infection. After intratracheal administration of justice plasmid expressing IL-17, the expression of IL-17 and its downstream effectors significantly increased, accompanied by increase in neutrophil count. The justice plasmid expressing IL-17 was intratracheally administered before acute pseudomonas aeruginosa lung infection, which significantly increased the expression of IL-17 and its downstream effectors (IL-1β, MIP-2 and G-CSF) in the respiratory tract, leading to increasing clearance rate of bacteria and survival rate.
IL-17 may recruit neutrophil to the infected areas in the early phase of pseudomonas aeruginosa lung infection.
铜绿假单胞菌可在免疫缺陷宿主中引起严重甚至致命的感染。白细胞介素-17（IL-17）是一种新发现的促炎细胞因子，它通过诱导趋化因子C-X-C的释放促进呼吸道中嗜中性粒细胞的募集和活化。
本研究旨在探讨IL-17在宿主抵御肺部急性铜绿假单胞菌感染中的作用。
检测急性铜绿假单胞菌感染小鼠肺中IL-17及其下游效应分子（IL-1β、MIP-2和G-CSF）的表达；气管内给予正义质粒48小时后，小鼠再次感染铜绿假单胞菌，6小时后测定细菌清除率、IL-17下游效应分子的表达以及小鼠死亡率。
急性铜绿假单胞菌感染小鼠肺中IL-17及其下游效应分子（IL-1β、MIP-2和G-CSF）的表达显著增加。气管内给予表达IL-17的正义质粒后，IL-17及其下游效应分子的表达显著增加，同时嗜中性粒细胞计数增加。在急性铜绿假单胞菌肺部感染前气管内给予表达IL-17的正义质粒，可显著增加呼吸道中IL-17及其下游效应分子（IL-1β、MIP-2和G-CSF）的表达，导致细菌清除率和存活率增加。
IL-17可能在铜绿假单胞菌肺部感染早期将嗜中性粒细胞募集到感染部位。
