Statin Decreases Burden in Macrophages by Promoting Autophagy.

Front Cell Infect Microbiol

Department of Microbiology and Immunology, Graduate Institute of Biomedical Sciences, College of Medicine, Chang Gung UniversityTaoyuan, Taiwan; Graduate Institute of Basic Medical Science, School of Medicine, China Medical UniversityTaichung, Taiwan; Department of Nursing, Asia UniversityTaichung, Taiwan; Department of Pediatrics, Molecular Infectious Disease Research Center, Chang Gung Children's Hospital and Chang Gung Memorial HospitalTaoyuan, Taiwan.

Published: September 2017

Statins, 3-hydroxy-3-methyl-glutaryl-coenzyme A (HMG-CoA) reductase inhibitors, have been found to provide protective effects against several bacterial infectious diseases. Although the use of statins has been shown to enhance antimicrobial treated eradication and reduce -mediated inflammation, the mechanisms underlying these effects remain unclear. In this study, and macrophage models were established to investigate the molecular pathways involved in statin-mediated inhibition of . -induced inflammation. Our study showed that statin treatment resulted in a dose-dependent decrease in intracellular . burden in both RAW264.7 macrophage cells and murine peritoneal exudate macrophages (PEMs). Furthermore, statin yielded enhanced early endosome maturation and subsequent activation of the autophagy pathway, which promotes lysosomal fusion resulting in degradation of sequestered bacteria, and in turn attenuates interleukin (IL)-1β production. These results indicate that statin not only reduces cellular cholesterol but also decreases the . burden in macrophages by promoting autophagy, consequently alleviating . -induced inflammation.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5239775PMC
http://dx.doi.org/10.3389/fcimb.2016.00203DOI Listing

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