Mucosal macrophage inflammatory protein‐1α activity in Helicobacter pylori infection

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Abstract
Mucosal chemokines are considered to be important in the pathogenesis of Helicobacter pylori‐associated gastritis. The aims of this study are to examine the levels of macrophage inflammatory protein‐1α (MIP‐1α) in organ cultures, the expression of MIP‐1α mRNA and the cellular source of MIP‐1α, using the antral mucosal specimens obtained from H. pylori‐positive and ‐negative patients. Enzyme‐linked immunosorbent assay was used to measure the levels of MIP‐1α in organ cultures of mucosal tissues and cell cultures of fractionated mucosal cells. The expression of MIP‐1α mRNA and protein was analysed in fresh biopsy tissues with reverse transcriptase–polymerase chain reaction (RT‐PCR) and double immunofluorescence microscopy, respectively. The mucosal specimens obtained from H. pylori‐positive patients exhibited significantly higher values of MIP‐1α activity in organ cultures with increased numbers of CD68+ macrophages, myeloperoxidase+ neutrophils and mononuclear cells in the lamina propria compared with those from H. pylori‐negative patients. The RT‐PCR analysis detected MIP‐1α mRNA in more than 50% of the specimens with H. pylori infection, but not in those without infection. In cell cultures, the macrophage fraction contained substantially higher amounts of MIP‐1α on a per cell basis than the lymphocyte fraction and MIP‐1α activity was not detected in cultures of gastric epithelial cells. This observation was also confirmed by a double immunofluorescence microscopic study in which most (> 90%) MIP‐1α‐positive infiltrating cells were CD68+ macrophages. This study indicates that synthesis and secretion of MIP‐1α are increased in H. pylori‐infected antral mucosa and that mucosal macrophages are the main cell type responsible for this phenomenon.