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Neuroinflammation mediated by microglia plays a key role in the pathogenesis of Parkinson's disease (PD), and our previous studies showed this was significantly inhibited by enhanced autophagy. In the autophagy pathway, Bcl2-associated athanogene (BAG)3 is a prominent co-chaperone, and we have shown BAG3 can regulate autophagy to clear the PD pathogenic protein α-synuclein. However, the connection between BAG3 and microglia mediated neuroinflammation is not clear.In this study, we explored whether BAG3 regulated related neuroinflammation and its original mechanism in PD. An inflammatory model of PD was established by injecting adeno-associated virus (AAV)-BAG3 into the bilateral striatum of C57BL/6 male mice to induce overexpression of BAG3, followed by injection of lipopolysaccharide (LPS). The striatum was extracted at 3 days after injection of LPS for Western blotting and reverse transcription quantitative polymerase chain reaction (RT-qPCR), and immunohistochemical staining was performed at 21 days after injection. At the same time, LPS was used to induce activation of BV2 cells to verify the effect of BAG3Overexpression of BAG3 reduced LPS-induced pyroptosis by reducing activation of caspase-1, the NOD-like receptor family, and the pyrin domain-containing 3 (NLRP3) inflammasome, and by release of interleukin (IL)-1β and tumor necrosis factor (TNF)-α. The LPS-induced inflammatory environment inhibits autophagy, and overexpression of BAG3 can restore autophagy, which may be the mechanism by which BAG3 reduces neuronal inflammation in PD.Our results demonstrate BAG3 promotes autophagy and suppresses NLRP3 inflammasome formation in PD.

This study assessed the epidemiology of sexually transmitted infections (STIs), HIV, and associated risk factors among female sex workers (FSWs) in Guangxi autonomous region, China. A cross-sectional study of 488 FSWs was conducted using a structured questionnaire to collect sociodemographic and behavioral information. Biological specimens from subjects were sampled to detect various STIs and HIV infection. Among FSWs, the prevalence rates of syphilis, Neisseria gonorrhoeae, Chlamydia trachomatis, genital herpes, condyloma acuminate, and HIV were 7.2%, 1.8%, 18.2%, 0.4%, 2.3%, and 0.8%, respectively. The prevalence rates of single, double, and triple infections were 22.3%, 3.9%, and 0.20%, respectively. Multivariate analysis indicated that STIs and HIV infection was independently related to low education level (OR = 7.244; 95% CI = 3.031-17.213; P0.001), low knowledge of STIs/HIV (OR = 0.191; 95% CI = 0.108-0.337; P0.001), low-grade working place (OR = 1.64; 95%CI = 1.016-2.648; P = 0.046), and no condom use during the last sexual intercourse (OR = 0.199; 95% CI = 0.113-0.350; P0.001). The prevalence of STIs is high among FSWs in Guangxi, is accompanied by a 0.8% HIV-positive rate, and may be largely related to high-risk sexual behaviors. Future interventions should be focused on the reduction of risk factors, including promotion of condom use and improvement of knowledge of STIs and HIV among FSWs.