Statin Decreases Helicobacter pylori Burden in Macrophages by Promoting Autophagy
نویسندگان
چکیده
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 Helicobacter pylori eradication and reduce H. pylori-mediated inflammation, the mechanisms underlying these effects remain unclear. In this study, in vitro and ex vivo macrophage models were established to investigate the molecular pathways involved in statin-mediated inhibition of H. pylori-induced inflammation. Our study showed that statin treatment resulted in a dose-dependent decrease in intracellular H. pylori 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 H. pylori burden in macrophages by promoting autophagy, consequently alleviating H. pylori-induced inflammation.
منابع مشابه
Role of autophagy associated with Helicobacter pylori CagA and VacA toxins in gastric cancer
Helicobacter pylori (H. pylori) is a gram-negative microaerophilic bacterium that has been introduced as a cause of mucosal inflammation and gastric cancer. The most important pathogenic factors are VacA and CagA, which are associated with increased disease severity in clinical strains. Autophagy is a protected lysosomal degradation pathway degrading cytoplasmic content and is important in host...
متن کاملComparing Serum Levels of Autophagy-Related Gene 5 in People With and Without Helicobacter Pylori Infection
Background: Laboratory studies have shown that gastric epithelial infection cells with Helicobacter pylori (H. pylori) can increase autophagy. Disruption in this process can cause various diseases, including cancer. Objective: This study aims to compare the serum level of Autophag -Related Gene 5 (ATG5) in individuals with and without H. pylori infection. Methods: This case-control pilot stud...
متن کاملMacrophages are mediators of gastritis in acute Helicobacter pylori infection in C57BL/6 mice.
Helicobacter pylori is the etiological agent of human chronic gastritis, a condition seen as a precursor to the development of gastrointestinal ulcers or gastric cancer. This study utilized the murine model of chronic H. pylori infection to characterize the role of macrophages in the induction of specific immune responses and gastritis and in the control of the bacterial burden following H. pyl...
متن کاملCompromised autophagy by MIR30B benefits the intracellular survival of Helicobacter pylori
Helicobacter pylori evade immune responses and achieve persistent colonization in the stomach. However, the mechanism by which H. pylori infections persist is not clear. In this study, we showed that MIR30B is upregulated during H. pylori infection of an AGS cell line and human gastric tissues. Upregulation of MIR30B benefited bacterial replication by compromising the process of autophagy durin...
متن کامل