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塞来昔布与环丙沙星联合治疗通过调节细胞因子平衡减轻活金黄色葡萄球菌诱导的小鼠小胶质细胞氧化损伤和炎症。

Combination treatment of celecoxib and ciprofloxacin attenuates live S. aureus induced oxidative damage and inflammation in murine microglia via regulation of cytokine balance.

机构信息

Department of Physiology, Immunology Laboratory, University of Calcutta, 92 A.P.C. Road, Calcutta 700009, West Bengal, India.

Department of Physiology, Immunology Laboratory, University of Calcutta, 92 A.P.C. Road, Calcutta 700009, West Bengal, India.

出版信息

J Neuroimmunol. 2018 Mar 15;316:23-39. doi: 10.1016/j.jneuroim.2017.12.006. Epub 2017 Dec 12.

DOI:10.1016/j.jneuroim.2017.12.006
PMID:29269130
Abstract

Microglial activation is the most common phenomenon in S. aureus induced brain abscesses as well as other common neurodegenerative diseases. The main objective of this study is to reduce the microglial inflammation with effective bacterial elimination. Ciprofloxacin and celecoxib were used in combination to regulate S. aureus induced oxidative stress and inflammation in primary murine microglial cells. Our results showed that combination treatment effectively killed viable S. aureus and reduced the inflammatory consequences. It can be concluded that lower production of pro-inflammatory cytokines and higher anti-inflammatory IL-10 level may be responsible for microglial polarization switching from pro-inflammatory M1 to anti-inflammatory M2.

摘要

小胶质细胞激活是金黄色葡萄球菌诱导性脑脓肿以及其他常见神经退行性疾病中最常见的现象。本研究的主要目的是通过有效的细菌消除来减轻小胶质细胞炎症。本研究采用环丙沙星和塞来昔布联合调节原代小鼠小胶质细胞中金黄色葡萄球菌诱导的氧化应激和炎症。结果表明,联合治疗能有效杀灭金黄色葡萄球菌活细胞,并减轻炎症后果。可以得出结论,促炎细胞因子产生减少和抗炎细胞因子 IL-10 水平升高可能是小胶质细胞从促炎 M1 向抗炎 M2 极化转换的原因。

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