The lamina propria of the gastric mucosa in the normal individual contains scattered B cells, plasma cells, and a small number of T cells. Intraepithelial T cells are also present but are less numerous than is seen in the small intestine. There is no organized lymphoid tissue in the form of MALT within the normal gastric mucosa. Immunohisto-chemical studies suggest that the normal gastric microenvironment is quiescent as there is no expression of antigens associated with inflammation such as epithelial HLA class II or CD25 (interleukin-2 receptor) on lamina propria macrophages or T lymphocytes (18).
As the normal stomach is a hostile environment for infective organisms, and the lamina propria is protected from luminal derived antigens by a thick layer of viscous mucus and an intact epithelium that is generally nonabsorptive and lacks M cells, there is little stimulation to lymphoid tissue. However, there are circumstances in which these barriers can be overcome, resulting in the stimulation of lymphoid tissue and the acquisition of MALT. This is most commonly seen in association with colonization of the stomach by H. pylori, an organism that is ideally adapted to living within the gastric environment associated with its motility, ability to penetrate the mucus layer and adhere to the gastric epithelium, and to secrete enzymes (in particular urease) that are active at low pH and that increase the local pH within the organism's microenvironment.
H. pylori infection is associated with a spectrum of abnormalities in the stomach. All patients infected by H. pylori have an abnormal gastric mucosa. Active chronic gastritis with neutrophil penetration predominantly of the superficial epithelium is maximal around the surface and neck regions, where the organism shows the highest concentration. In many instances, the neutrophils and H. pylori organisms are spatially related. Infiltration of the epithelium by acute inflammatory cells is likely to cause damage to the integrity of the epithelial barrier and to result in the potential leak of antigen into the lamina propria and stimulation of lymphoid tissue. This has been confirmed by studying gastric permeability to sucrose, which is higher in patients with H pylori infection (19) and which normalizes after eradication of the organism (20). Increased permeability of the epithelium together with the presence of H. pylori-derived antigens may be responsible for the subsequent acquisition of MALT within the gastric mucosa.
Several studies have shown that infection with H. pylori is associated with the accumulation of MALT within the stomach. Although lymphoid follicles are not found in endoscopic biopsies from normal individuals (13,14,16), they can be found in 27-100% of patients infected with H. pylori (13-16). In the most comprehensive study, Genta et al. (16) demonstrated that lymphoid follicles can be detected in all patients with H. pylori infection if the biopsies are sufficiently large and numerous. Wotherspoon et al. (15) showed that the lymphoid tissue that accumulates in H. pylori infection has features of MALT, with the formation of a lymphoepithelium by the marginal zone B cells around the follicles that infiltrated the foveolar epithelium of the gastric glands.
Although H. pylori is probably the most common association with acquired gastric MALT, it is not the only stimulus to accumulation of lymphoid tissue in the gastric mucosa. The related organism Helicobacter heilmannii is also associated with acquired gastric MALT (21), and MALT-type lymphoid tissue has been described in the stomachs of patients with celiac disease.
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