Altered expression of membrane inhibitors of complement in human gastric epithelium during Helicobacter‐associated gastritis

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Abstract
Aims: Membrane inhibitors of complement are thought to protect bystander cells from complement mediated damage. Expression of these proteins is enhanced in the colonic mucosa of patients with ulcerative colitis. Our aim was to investigate the regulation of complement activity in Helicobacter‐associated chronic gastritis.Methods and results: We immunohistochemically assayed expression of three membrane inhibitors of complement, decay accelerating factor (DAF; CD55), 20 kDa homologous restriction factor (HRF20; CD59) and membrane cofactor protein (MCP; CD46), in 55 biopsy specimens of the human gastric mucosa. DAF, expressed in 33 (60%) of biopsy specimens, and HRF20, expressed in 45 (82%) of the samples, were located mainly on the apical surface of the epithelial cells, whereas MCP, expressed in 48 (87%) of the biopsies, was found on the basolateral surface. We found strong correlation between expression of DAF on gastric mucosal epithelium and the severity of mucosal infiltration of neutrophils (rs = 0.875, P < 0.0001) and mononuclear cells (rs = 0.773, P < 0.0001). No significant correlation was observed between HRF20 expression and neutrophil or mononuclear cell infiltration, while there was a weak negative correlation between MCP expression and these cellular infiltrations. When we assayed immunostaining of Helicobacter pylori (H. pylori) in these biopsy specimens, strong correlation with the degree of neutrophil (P < 0.0001) and mononuclear cell (P < 0.0001) infiltration were observed. The expression of DAF and H. pylori infection in these biopsies were also significantly (P < 0.0001) correlated. No correlation between HRF20 expression and H. pylori infection was observed, but we did find a significant negative correlation (P < 0.005) between the expression of MCP and H. pylori infection.Conclusions: Our results, demonstrating altered expression of membrane inhibitors of complement in gastric mucosa during inflammation and/or H. pylori infection, suggest that complement may significantly participate in the pathology of gastric inflammation. Moreover, DAF and MCP may play an important role in the regulation of complement activation in the alimentary tract.

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