1998 Volume 6 Issue 2 Pages 73-79
Helicobacter pylori (HP)-provoked chronic active gastritis is histologically featured by regeneration/hyperplasia of foveolar cells, dense infiltration of lymphoid cells and neutrophils, and formation of lymphoid follicles. Mucosal areas with intestinal metaplasia are consistently devoid of HP infection. When bacilliform or coccoid bacteria are seen on the surface of the foveolar cells (within the mucus gel layer), we can regard them as HP. Exceptions are H. felis and Gastrospillirum hominis, seen as heavily coiled, long spiral bacteria.
Histochemical techniques for identifying HP in gastric biopsy specimens include Giemsa, Warthin-Starry and Genta stains, the immunostain using polyclonal or monoclonal antibodies, and nonisotopic in situ hybridization histochemistry. The most practical and convenient method we recommend is a modified hematoxylin and eosin stain, in which the hematoxylin staining time should simply be prolonged double (e. g. from 5min to 10min).
We have hypothesized that intestinal metaplasia represents a specific local immune response (adaptation) of the gastric mucosa to persistent HP infection. Intestinal metaplasia is quite active in secreting HP-specific secretory IgA, which may clear HP off the surface of metaplastic epithelia, resulting in the withdrawal of inflammatory cells and the disappearance of lymphoid follicles from the lamina propria. IgG-containing plasma cells, densely distributed in non-metaplastic gastritis, are scarcely seen within the metaplastic mucosa. A supportive immunochemical study has demonstrated that HP-specific secretory IgA is richly detected in the gastric secretion in cases with marked atrophic (metaplastic) gastritis.
The number of IgE-containing plasma cells in HP-infected gastric mucosa is higher than those in HP-negative mucosa. In addition, we occasionally observe IgE-positivity along the dendritic cells in the germinal center of lymphoid follicles formed in the HP-infected gastric mucosa. Monoclonal antibodies to bacterial heat shock protein 60 are cross-reactive with the gastric foveolar cells and germinal center lymphocytes, although the incidence of epithelial positivity was not significantly different between HP-infected and HP-free gastric mucosae. These findings may suggest an allergic/autoimmune response to HP or HP-infected epithelia in HP-induced gastritis.
We have reported that two types of benign gastric lesions may be provoked by local lamina proprial penetration of HP. These include gastric xanthomas and so-called "Russell body gastritis". HP antigens can immunohistochemically be detected in the cytoplasm of macrophages accumulated within these lesions.
