title: Effects of SCR-3 on the immunosuppression accompanied with the systemic inflammatory response syndrome.
abstract: Steroid receptor coactivator-3 (SRC-3) is a multifunctional protein that plays an important role in mammary gland growth, development, and tumorigenesis. In this study, SCR-3 gene knockout mice were used to study the effects of SCR-3 on the immunosuppression accompanied with systemic inflammatory response syndrome (SIRS). Bacterial clearance assay was performed by blood culture and frozen sections, and the results showed that the absence of SCR-3 protein serious damaged the innate immune system and the body's ability to inactivate or phagocytosis of bacteria was significantly decreased, and the absence of SCR-3 protein also weakened phagocytes' ability to degrade bacteria and their metabolites. Furthermore, animal model of inflammatory reaction was established and the immune function was determined, and the results revealed that SRC-3 protein may play an important role in maintenance of T-cells' immune function, and severe T-cell immune function disorder would be resulted once SRC-3 protein is missing. In addition, the results of our study showed the steady-state of lymphocyte subsets was destroyed after SIRS, leading the suppression of cellular immune function, and the absence of SCR-3 protein may aggravate the suppression of T-lymphocyte function. Therefore, the present study demonstrated that the absence of SCR-3 protein would aggravate immunosuppression. In addition, SRC-3 protein is a significant regulator of infection and inflammation, and SRC-3 protein play an essential role in the development of immunosuppression accompanied with SIRS.
authors.affiliation: Department of Anesthesia, General Hospital of Chengdu Military Command Area, Chengdu 610083, Sichuan Province, People's Republic of China.
authors.forename: Jun
authors.initials: J
authors.lastname: Li
authors.forename: Jie
authors.initials: J
authors.lastname: Niu
authors.forename: Shan
authors.initials: S
authors.lastname: Ou
authors.forename: Zhan-Yong
authors.initials: ZY
authors.lastname: Ye
authors.forename: Deng-Qun
authors.initials: DQ
authors.lastname: Liu
authors.forename: Feng-Chao
authors.initials: FC
authors.lastname: Wang
authors.forename: Yong-Ping
authors.initials: YP
authors.lastname: Su
authors.forename: Jun-Ping
authors.initials: JP
authors.lastname: Wang
mesh_terms: D000818:Animals; D001419:Bacteria / Q000472:pathogenicity; D005260:Female; D007113:Immunity, Innate / Q000235:genetics; D007376:Interleukin-2 / Q000097:blood; D008070:Lipopolysaccharides / Q000008:administration & dosage; D016131:Lymphocyte Subsets / Q000187:drug effects / Q000276:immunology; D051379:Mice; D018345:Mice, Knockout; D056921:Nuclear Receptor Coactivator 3 / Q000172:deficiency / Q000235:genetics / Q000276:immunology*; D010587:Phagocytosis / Q000235:genetics; D018746:Systemic Inflammatory Response Syndrome / Q000097:blood / Q000235:genetics / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology* / Q000473:pathology
chemical_list: D007376:Interleukin-2; D008070:Lipopolysaccharides; C538867:Ncoa3 protein, mouse; D056921:Nuclear Receptor Coactivator 3