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Published on: February 9, 2014
[Effect of carbachol on dendritic cell function in the lipopolysaccharides induced murine sepsis model]
Guang Tian1, Jiang-yang Lu, Sen Hu
1Department of Pathology, Burn Institute, First Affiliated Hospital of General Hospital of PLA, Beijing 100037, China.
Objective:
To explore the mechanism of the effect of carbachol in the treatment of sepsis at the angle of modulation of dendritic cell (DC) activity.
Methods:
Thirty male C57BL/6 mice were randomized into three groups: normal control, sepsis and carbachol. The sepsis model of mice was reproduced by the injection of lipopolysaccharides (LPS). The expression of interleukin-1 beta (IL-1 beta) and IL-12 p70 positive cells were measured by immunohistochemistry method. The changes in DC activity in the spleen of mice were studied using flow cytometry.
Results:
In LPS group, the number of splenic DC was increased, but it was not statistically significant. The expression of DC molecules including major histocompatibility complex-II (MHC-II), CD86 and the rate of positive cells containing IL-1 beta and IL-12 p70 were significantly higher than those in normal controls (all P<0.05). While in carbachol treatment group, the number of splenic DC had no significant change, the expression of IL-1 beta was down-regulated, dramatically. The expression of MHC-II, CD86 and IL-12 p70 were also lowered (all P<0.05).
Conclusion:
Carbachol can lower the DC activity, suggesting that modulation of DC activity may lower extensive immune and inflammatory response in the early phases of sepsis.
