title: Thymosin-alpha1 promotes the apoptosis of regulatory T cells and survival rate in septic mice.
abstract: Tregs are involved in immune disorder during sepsis; they can lead to a Th2 immune reaction. Their inhibitory effects can help alleviate inflammatory injury, but may also cause secondary immune inhibition. Thymosin-alpha1 is a polypeptide with powerful immunomodulatory activities. Current reports have shown that Thymosin-alpha1 conferred beneficial effects to septic patients. To explore the relationship between Thymosin-alpha1 and Tregs, in this study, we investigated the changing trend in CD4(+)CD25(+)Foxp3(+) T lymphocytes in a CLP septic mouse model. We also investigated the variation of apoptotic rate of CD4(+)CD25(+) T lymphocytes, cytokine variation, and change of model survival rate when Thymosin-alpha1 intervening or not. We observed that the 72-h survival rate was improved, the percentage of CD4(+)CD25(+)Foxp3(+) T lymphocytes decreased and the apoptosis rate of CD4(+)CD25(+) T lymphocytes increased after intervention of Thymosin-alpha1. At same time the expression of pro-inflammation cytokines IL-2, TNF-alpha and anti-inflammatory cytokines IL-10 and TGF-beta were regulated. In conclusion, Thymosin-alpha1 can effectively control the inflammatory response intensity and improve the 72-h survival rate of septic mice. Regulating Tregs may be another important role of Thymosin-alpha1 conditioning the immune reaction in sepsis.
authors.affiliation: Department of emergency and critical care medicine, Shanghai Changzheng Hospital, The Second Military Medical University, Shanghai, 200003, China.
authors.forename: Jian
authors.initials: J
authors.lastname: Wan
authors.forename: Yi
authors.initials: Y
authors.lastname: Shan
authors.forename: Hongwei
authors.initials: H
authors.lastname: Shan
authors.forename: Guomin
authors.initials: G
authors.lastname: Li
authors.forename: Tao
authors.initials: T
authors.lastname: Wang
authors.forename: Jun
authors.initials: J
authors.lastname: Guan
authors.forename: Xuefeng
authors.initials: X
authors.lastname: Liu
authors.forename: Dechang
authors.initials: D
authors.lastname: Chen
authors.forename: Wenfang
authors.initials: W
authors.lastname: Li
authors.forename: Zhaofen
authors.initials: Z
authors.lastname: Lin
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D016207:Cytokines / Q000097:blood; D004195:Disease Models, Animal; D051858:Forkhead Transcription Factors / Q000378:metabolism; D007082:Ileum / Q000473:pathology; D007155:Immunologic Factors / Q000494:pharmacology; D051379:Mice; D018805:Sepsis / Q000188:drug therapy* / Q000276:immunology / Q000473:pathology; D016176:T-Lymphocyte Subsets / Q000187:drug effects / Q000276:immunology / Q000473:pathology; D050378:T-Lymphocytes, Regulatory / Q000187:drug effects* / Q000276:immunology / Q000473:pathology; D000077596:Thymalfasin; D013947:Thymosin / Q000031:analogs & derivatives* / Q000276:immunology / Q000494:pharmacology
chemical_list: D016207:Cytokines; D051858:Forkhead Transcription Factors; C498833:Foxp3 protein, mouse; D007155:Immunologic Factors; D013947:Thymosin; D000077596:Thymalfasin