Helicobacter pylori infection up-regulates gland mucous cell-type mucins in gastric pyloric mucosa.

Abstract

Two types of mucous cell are present in gastric mucosa: surface mucous cells (SMCs) and gland mucous cells (GMCs), which consist of cardiac gland cells, mucous neck cells, and pyloric gland cells. We have previously reported that the patterns of glycosylation of SMC mucins are reversibly altered by Helicobacter pylori infection. In this study, we evaluated the effects of H. pylori infection on the expression of GMC mucins in pyloric gland cells. Gastric biopsy specimens from the antrums of 30 H. pylori-infected patients before and after eradication of H. pylori and 10 normal uninfected volunteers were examined by immunostaining for MUC6 (a core protein of GMC mucins), alpha1,4-N-acetyl-glucosaminyl transferase (alpha4GnT) (the glycosyltransferase which forms GlcNAcalpha1-4Galbeta-R), and GlcNAcalpha1-4Galbeta-R (a GMC mucin-specific glycan). MUC6, alpha4GnT, and HIK1083-reactive glycan were expressed in the cytoplasm, supranuclear region, and secretory granules in pyloric gland cells, respectively. The immunoreactivity of MUC6 and alpha4GnT, but not of GlcNAcalpha1-4Galbeta-R, in the pyloric gland increased in H. pylori-associated gastritis, and after the eradication of H. pylori, the increased expression of MUC6 and alpha4GnT in the gastric mucosa of H. pylori-infected patients decreased to almost normal levels. This up-regulation was correlated with the degree of inflammation. In addition to the synthesis of GMC mucins increasing reversibly, their metabolism or release may also increase reversibly in H. pylori-associated gastritis. The up-regulation of the expression of gastric GMC mucins may be involved in defense against H. pylori infection in the gastric surface mucous gel layer and on the gastric mucosa.