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Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 J+Immunol 2013 ; 190 (12): 6626-34 Nephropedia Template TP
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H pylori Infection Inhibits Phagocyte Clearance of Apoptotic Gastric Epithelial Cells #MMPMID23686492
Bimczok D; Smythies LE; Waites KB; Grams JM; Stahl RD; Mannon PJ; Peter S; Wilcox CM; Harris PR; Das S; Ernst PB; Smith PD
J Immunol 2013[Jun]; 190 (12): 6626-34 PMID23686492show ga
Increased apoptotic death of gastric epithelial cells is a hallmark of H. pylori infection, and altered epithelial cell turnover is an important contributor to gastric carcinogenesis. To address the fate of apoptotic gastric epithelial cells and their role in H. pylori mucosal disease, we investigated phagocyte clearance of apoptotic gastric epithelial cells in H. pylori infection. Human gastric mononuclear phagocytes were analyzed for their ability to take up apoptotic epithelial cells in vivo using immunofluorescence analysis. We then used primary human gastric epithelial cells induced to undergo apoptosis by exposure to live H. pylori to study apoptotic cell uptake by autologous monocyte-derived macrophages. We show that HLA-DR+ mononuclear phagocytes in human gastric mucosa contain cytokeratin-positive and TUNEL-positive apoptotic epithelial cell material, indicating that gastric phagocytes are involved in apoptotic epithelial cell clearance. We further show that H. pylori both increased apoptosis in primary gastric epithelial cells and decreased phagocytosis of the apoptotic epithelial cells by autologous monocyte-derived macrophages. Reduced macrophage clearance of apoptotic cells was mediated in part by H. pylori-induced macrophage TNF-?, which was expressed at higher levels in H. pylori-infected, compared to uninfected, gastric mucosa. Importantly, we show that H. pylori-infected gastric mucosa contained significantly higher numbers of apoptotic epithelial cells and higher levels of non-phagocytosed TUNEL-positive apoptotic material, consistent with a defect in apoptotic cell clearance. Thus, as shown in other autoimmune and chronic inflammatory diseases, insufficient phagocyte clearance may contribute to the chronic and self-perpetuating inflammation in human H. pylori infection.