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布洛芬在创伤弧菌感染小鼠模型中增强促炎细胞因子释放。

Ibuprofen augments pro-inflammatory cytokine release in a mouse model of Vibrio vulnificus infection.

作者信息

Lee Yuarn-Jang, Chuang Yin-Ching

机构信息

Section of Infectious Diseases, Department of Internal Medicine, Taipei Medical University Hospital, 252 Wu Hsing Street, Taipei, Taiwan.

出版信息

Microbiol Immunol. 2010 Sep;54(9):542-50. doi: 10.1111/j.1348-0421.2010.00249.x.

DOI:10.1111/j.1348-0421.2010.00249.x
PMID:20840153
Abstract

We evaluated the effects of ibuprofen on cytokine production and mortality in a mouse model of septic shock induced by Vibrio vulnificus, strain Chi Mei Vv05191. Ibuprofen (50 mg/kg) or saline (control) was given to female BALB/cByJ mice for three consecutive days before exposure to the pathogen. For cytokine production, serum and peritoneal fluid were assayed for IL-1β, IL-6, TNF-α, and MIP-2 by ELISA at 3, 6, and 9 hr after intraperitoneal infection of the organism. At 6 hr after infection, serum and peritoneal fluid levels of IL-6, TNF-α, and MIP-2 were significantly higher in the ibuprofen group. For mortality determination, 73 mice (37 ibuprofen, 36 control) were injected intramuscularly with V. vulnificus. Kaplan-Meier survival curves were analyzed. Survival was significantly decreased by ibuprofen only for the lowest inoculum (25 CFU) of V. vulnificus. Administration of ibuprofen before infection may augment the pathogenesis of V. vulnificus by stimulating cytokine production.

摘要

我们评估了布洛芬对创伤弧菌(菌株Chi Mei Vv05191)诱导的脓毒症休克小鼠模型中细胞因子产生及死亡率的影响。在暴露于病原体之前,连续三天给雌性BALB/cByJ小鼠注射布洛芬(50 mg/kg)或生理盐水(对照)。对于细胞因子产生情况,在腹腔感染该病原体后3、6和9小时,通过酶联免疫吸附测定法(ELISA)检测血清和腹腔液中的白细胞介素-1β(IL-1β)、白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)和巨噬细胞炎性蛋白-2(MIP-2)。在感染后6小时,布洛芬组血清和腹腔液中IL-6、TNF-α和MIP-2的水平显著更高。为了确定死亡率,给73只小鼠(37只注射布洛芬,36只作为对照)肌肉注射创伤弧菌。分析了Kaplan-Meier生存曲线。仅对于最低接种量(25个菌落形成单位)的创伤弧菌,布洛芬会显著降低生存率。感染前给予布洛芬可能通过刺激细胞因子产生而增强创伤弧菌的致病作用。

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