TRIM32 Drives Pathogenesis in Streptococcal Toxic Shock-Like Syndrome and Streptococcus suis Meningitis by Regulating Innate Immune Responses
Xuan Ouyang, Jie Guo, Qingyu Lv, Hua Jiang, Yuling Zheng, Peng Liu, Tongyan Zhao, Decong Kong, Huaijie Hao, Yongqiang Jiang
Abstract
Streptococcus suis is an emerging zoonotic agent that causes streptococcal toxic shock-like syndrome (STSLS) and meningitis in humans, with high mortality and morbidity. The pathogenesis of both STSLS and central nervous system (CNS) infections caused by S. suis is not well understood. TRIM32, a member of the tripartite motif (TRIM) protein family, has been reported to regulate host inflammatory responses. In this study, we showed that TRIM32 deficiency significantly reduced the level of bacteremia and the production of proinflammatory cytokines following severe S. suis infection, protecting infected mice from STSLS.
Topics & Concepts
Innate immune systemBiologyStreptococcus suisPathogenesisMeningitisMicrobiologyImmunologyStreptococcaceaeImmune systemToxic shock syndromeStreptococcusStreptococcus agalactiaeStreptococcus pneumoniaeImmunityShock (circulatory)BacteriaAntibioticsMedicineVirulenceStaphylococcus aureusGenePsychiatryGeneticsBiochemistryInternal medicineStreptococcal Infections and TreatmentsInflammasome and immune disordersBacterial Infections and Vaccines