Open AccessTRIM32 Drives Pathogenesis in Streptococcal Toxic Shock-Like Syndrome and Streptococcus suis Meningitis by Regulating Innate Immune Responses
Author(s) -
Xue Ouyang,
Jie Guo,
Qingyu Lv,
Hua Jiang,
Yinan Zheng,
Peng Liu,
Tongyan Zhao,
Decong Kong,
Huaijie Hao,
Yongqiang Jiang
Publication year - 2020
Publication title -
infection and immunity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.508
H-Index - 220
eISSN - 1070-6313
pISSN - 0019-9567
DOI - 10.1128/iai.00957-19
Subject(s) - streptococcus suis , pathogenesis , biology , immunology , proinflammatory cytokine , meningitis , innate immune system , toxic shock syndrome , immune system , microbiology and biotechnology , bacteremia , inflammation , medicine , bacteria , antibiotics , virulence , gene , staphylococcus aureus , genetics , psychiatry
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. The influence of TRIM32 gene deletion on a range of processes known to be involved in S. suis meningitis was also examined. Both levels of bacterial loads and indications of brain hemorrhage were reduced in infected Trim32 - / - mice compared with infected wild-type (WT) controls. We also found that TRIM32 deficiency increased the permeability of the blood-brain barrier (BBB) and the recruitment of inflammatory monocytes during the early course of S. suis infection, potentially limiting the development of S. suis meningitis. Our results suggest that TRIM32 sensitizes S. suis -induced infection via innate immune response regulation.