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可能的氯霉素在 TSST-1 和凝固酶阳性金黄色葡萄球菌诱导的关节炎中的保护作用,炎症介质水平改变。

Possible protective role of chloramphenicol in TSST-1 and coagulase-positive Staphylococcus aureus-induced septic arthritis with altered levels of inflammatory mediators.

机构信息

Immunology Laboratory, Department of Physiology, University Colleges of Science and Technology, University of Calcutta, Calcutta, West Bengal 700009, India.

出版信息

Inflammation. 2011 Aug;34(4):269-82. doi: 10.1007/s10753-010-9233-0.

Abstract

Chloramphenicol is mostly used against coagulase-negative Staphylococcus aureus, and its protective role against coagulase-positive S. aureus is not well studied. In our study, arthritis was induced in mice by S. aureus (Apollo Gleneagles 33 (AG-33) or American Type Culture Collection 25923 (ATCC-25923)) infection. Chloramphenicol was administered after 2 h of infection. Mice were killed at 1, 3, 5 days post-infection. Mice inoculated with pathogenic Staphylococci (AG-33) expressing coagulase and Toxic shock syndrome toxin-1 (TSST-1), displayed severe arthritis with enhanced bacterial burden in the spleen, cytokine production in serum and synovial tissue, neutrophil recruitment, and cyclooxegenase-2 expression in synovial tissue compared with ATCC-25923-infected groups. Severity of arthritis was regulated by chloramphenicol treatment. Our study suggests that alteration in the inflammatory cytokine levels and pronounced production of cyclooxygenase-2 play important roles in progression of arthritis which is regulated by application of chloramphenicol.

摘要

氯霉素主要用于治疗凝固酶阴性葡萄球菌感染,而其对凝固酶阳性葡萄球菌的保护作用尚未得到充分研究。在我们的研究中,通过金黄色葡萄球菌(Apollo Gleneagles 33(AG-33)或美国模式培养物集存库 25923(ATCC-25923))感染诱导小鼠关节炎。在感染后 2 小时给予氯霉素。在感染后 1、3、5 天处死小鼠。接种表达凝固酶和中毒性休克综合征毒素 1(TSST-1)的致病性葡萄球菌(AG-33)的小鼠,与感染 ATCC-25923 的小鼠相比,出现严重关节炎,脾脏细菌负荷增加,血清和滑膜组织细胞因子产生增加,中性粒细胞募集增加,滑膜组织中环氧化酶-2 表达增加。关节炎的严重程度受氯霉素治疗的调节。我们的研究表明,炎症细胞因子水平的改变和环氧化酶-2 的显著产生在关节炎的进展中起重要作用,而氯霉素的应用可调节关节炎的进展。

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