Mast cells play a crucial role in Staphylococcus aureus peptidoglycan-induced diarrhea

被引:65
作者
Feng, Bai-Sui
He, Shao-Heng
Zheng, Peng-Yuan
Wu, Linda
Yang, Ping-Chang
机构
[1] McMaster Univ, Dept Pathol, Hamilton, ON L8N 4A6, Canada
[2] Nanjing Univ, Affiliated Hosp 1, Clin Expt Ctr, Nanjing, Jiangsu, Peoples R China
[3] Zhengzhou Univ, Hosp 2, Dept Gastroenterol, Zhengzhou, Peoples R China
基金
加拿大健康研究院;
关键词
D O I
10.2353/ajpath.2007.061274
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
Bacterium-induced diarrhea results in 2 to 2.5 million deaths in the world each year. The mechanism needs to be further understood. Staphylococcus aureus infection has a close relation with diarrhea; its cell wall component peptidoglycan (PGN) has strong biological activity on immune cells and possibly plays a role in S. aureus-induced diarrhea. The present study showed that oral PGN-induced diarrhea in mice in a dose-dependent manner. Intestinal epithelial cells absorbed PGN via the intracellular pathway. Intestinal mast cells were activated after PGN gavage. Toll-like receptor (TLR)2 expression was detected in mast cells in the intestine as well as in the murine mast cell line p815 cells. Blocking TIR2 or nucleotide-binding oligomerization domain (NOD)1 with related antibodies or RNA interference abolished PGN-induced p815 cell activation. The mast cell mediator histamine and serotonin had synergistic effects in PGN-induced diarrhea. In summary, oral PGN can induce diarrhea in mice, and TLR2 and NODI mediate the PGN-induced mast cell activation that plays a critical role in diarrhea induction. Blockade of TLR2 or NOD1 or treating mice with a mast cell stabilizer can efficiently inhibit PGN-induced-diarrhea, providing potential therapeutic significance.
引用
收藏
页码:537 / 547
页数:11
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