期刊
JOURNAL OF LEUKOCYTE BIOLOGY
卷 108, 期 5, 页码 1615-1629出版社
OXFORD UNIV PRESS
DOI: 10.1002/JLB.3MA0720-682RR
关键词
autophagy; flavonoids; inflammation; macrophages
资金
- State Key Laboratory of Research on Bioactivities and Clinical Applications of Medicinal Plants
- CUHK from Innovation and Technology Commission, Hong Kong
- Li Dak Sum Yip Yio Chin R & D Centre for Chinese Medicine, The Chinese University of Hong Kong
Tuberculosis (TB), a highly infectious air-borne disease, has remained a global health problem. Conventional treatment and preventions such as antibiotics and Bacilli Calmette-Guerin (BCG) vaccine can be unreliable. In view of the increasing prevalence of anti-TB drug resistance, adjunctive therapy may be necessary to shorten the recovery time. We have previously shown that flavonoids in the medicinal herbSophora flavescensexhibit anti-inflammatory and bactericidal activities. The aim of this study was to investigate the molecular and cellular characteristics of flavonoids ofS. flavescens(FSF) in BCG-stimulated macrophages for assessing their roles in anti-inflammation and autophagy. Mouse alveolar macrophage (MH-S) cell line and primary mouse peritoneal macrophages were stimulated in vitro with heat-inactivated BCG and treated with FSF, with or without autophagy inhibitor Bafilomycin A1 (BafA1). Gene expression was analyzed using quantitative PCR, and cytokine/chemokine release was analyzed by Milliplex assay and ELISA. Autophagy-related proteins were quantified by Western blot and flow cytometry, and autophagolysosomes were detected using fluorescence microscopy. In both MH-S cell line and mouse peritoneal macrophages stimulated by heat-inactivated BCG, FSF was found to up-regulate autophagy-related proteins microtubule-associated protein 1A/1B-light chain 3 (LC3) and protein 62 (p62), and suppress the induced proinflammatory cytokine TNF-alpha, CCL5, and IL-6. FSF actively modulates immune processes through suppressing BCG-mediated inflammation by promoting autophagy in MH-S cells and mouse peritoneal macrophages. We suggest that FSF may be useful as an adjunctive therapeutic agent for TB infection by modulating cell survival through autophagy and reducing inflammation.
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