The influence of 18% TBSA fullthickness scalding on murine splenic T lymphocyte phosphoinositide-specific PLC signal pathway and its function
- VernacularTitle:18%III度烫伤对小鼠脾脏T淋巴细胞肌醇脂质信号系统及其功能的影响
- Author:
Junsong ZHENG
;
Daizhi PENG
;
Jun WU
- Publication Type:Journal Article
- Keywords:
T lymphocyte PI-PLC pathway Signal transduction Burn
- From:
Chinese Journal of Immunology
1999;0(12):-
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the changes of postburn activity on murine splenic T lymphocyte phosphoinositide-specific PLC signal pathway, and look for the relationship between the postburn and T cell function suppression, IL-2 and IL-10 secretion.Methods:The experimental model was 18% TSBA (total body surface area) fullthickness scalded mice by vapor. The activities of G-protein, PTK (membrane, cytoplasmic) PKC (membrane, plasmic),PI-PLC and cytoplasmic free calcium concentration were detected at different postburn periods, moreover T lymphocyte proliferating function, IL-2 and IL-10 secretion were examined.Results:Compared with control group, membrane GTPase and plasmic PI-PLC enzyme were suppressed after scalded, calcium concentration lowered down significantly, the activities of PTK and PKC were complex, membrane PKC activity elevated after decreasing, those of plasmic PKC were just on the contrary, and the total activity of membrane and plasmic PKC was not stable; Membrane PTK activity decreased in the postburn early stage, then increasing.T cells proliferating function and IL-2 production marginally reduced, and the depressed levels of IL-2 production and T cells proliferating activity were positive parallel with the activities of G-protein and Ca ++. Cytoplasmic PKC activity lowered down after elevating, which was just negative linearly correlated with IL-10 secretion.Conclusion:Inhibition of G-protein ?PTK and Ca ++ activities in phosphoinositide-specific PLC signal pathway was the main reason which resulted in the decrease of IL-2 secretion, suppressed T cell proliferation and the dual-directional changes in IL-10 secretion.
