Xilin Xu1, Bing Shao2, Ran Wang3, Sijing Zhou4, Zhongzhi Tang1, Weihua Lu1, Shengdao Xiong5. 1. Department of Emergency Medicine, Wuhan General Hospital of Guangzhou Military Command Wuhan 430070, China. 2. Tongji Medical College, Huazhong University of Science and Technology Wuhan 430030, China. 3. Department of Respiratory Medicine, First Affiliated Hospital of Anhui Medical University Hefei 230001, China. 4. Department of Occupational Medicine, Hefei Third People's Hospital Hefei 230001, China. 5. Department of Respiratory Medicine, Tongji Hospital of Tongji Medical College, Huazhong University of Science and Technology Wuhan 430030, China.
Abstract
BACKGROUND: 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. OBJECTIVE: This study was conducted to explore the role of IL-17 in host defense against acute pseudomonas aeruginosa infection in lungs. METHODS: 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. RESULTS: 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. CONCLUSION: IL-17 may recruit neutrophil to the infected areas in the early phase of pseudomonas aeruginosa lung infection.
BACKGROUND: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. OBJECTIVE: This study was conducted to explore the role of IL-17 in host defense against acute pseudomonas aeruginosa infection in lungs. METHODS: 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. RESULTS: 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. CONCLUSION:IL-17 may recruit neutrophil to the infected areas in the early phase of pseudomonas aeruginosa lung infection.
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