Immunology Laboratory, Department of Physiology, University Colleges of Science and Technology, University of Calcutta, Calcutta, West Bengal 700009, India.
Inflammation. 2011 Aug;34(4):269-82. doi: 10.1007/s10753-010-9233-0.
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.
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。
