Some sulfated polysaccharides, such as d-CGN, APS, and DSS, have carcinogenicity to the rat colorectum. These materials first induced colitis, secondly squamous metaplasia, and finally tumors at the colorectum. Initially, colitis was located in the columnar epithelium of the rectum and extended proximally thereafter. Squamous metaplasia persisted in almost all experimental rats and progressed irreversibly. The tumors were adenoma, adenocarcinoma, squamous cell papilloma, and squamous cell carcinoma. Macrophages containing these materials were observed in the lamina propria mucosa and submucosa of the colorectum. There were differences in the molecular weight of the substances and their tumor incidences. However, with regard to their carcinogenicity, these sulfated polysaccharides were inferred to be similar to each other in their target organs and process of tumor development. Consequently, these sulfated polysaccharides may be one entity of carcinogenic sulfates.

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We have evaluated the use of proteinase K (PK)-treated cells isolated from Helicobacter pylori as lipopolysaccharide (LPS) antigens in an immunoblot assay and an enzyme-linked immunosorbent assay (ELISA) for the serodiagnosis of H. pylori infection. The sera from patients with chronic gastritis, gastric ulcer, duodenal ulcer or gastric cancer, and from healthy adults with or without H. pylori infection were assayed with three commercial serodiagnostic kits (HM-CAP, Helico-G, and G.A.P. II) and novel methods relying on the use of PK-treated cells. The PK-treated cells used in these assays were selected on the basis of their possibility to possess a common epitope in the 0-polysaccharides of H. pylori, which is known to be highly immunogenic in humans. Of the sera from these patients, 71-94% were positive with the commercial kits, 97 % with immunoblot assay, and 90% with ELISA. On the other hand, of the healthy adults infected with H. pylori, 72-97% were positive with the commercial kits, 86% with immunoblot assay, and 72% with ELISA. PK-treated cells that did not contain the common epitope were unsuitable as an antigen for immunoblot assay or ELISA. Furthermore, the reactivity of these sera reacted specifically with H. pylori PK-treated cells but not with LPSs from other gram-negative bacteria, such as Campylobacter, Proteus, Bordetella, and Salmonella. These results demonstrate that the serological assays relying on the use of H. pylori PK-treated cells possessing a highly antigenic epitope are potentially useful as a serodiagnostic test for H. pylori infection.

Helicobacter pylori and HLA-DR antigen expression on gastric epithelium, identified by an indirect immunoperoxidase staining method using monoclonal antibodies against H. pylori and HLA-DR antigens, were studied topographically. Fifty-nine biopsy specimens from 41 patients who had neither gastric cancer nor peptic ulcers were examined. H. pylori was observed predominantly over or on the surface epithelium, while HLA-DR antigens were frequently expressed on the epithelium of the isthmus region. These observations led to the conclusion that there was no direct topographic association between H. pylori and epithelial HLA-DR expression. However, the frequency of HLA-DR expression in H. pylori-positive (28/29) specimens was significantly higher than that in H. pylori-negative (18/30) specimens (P < 0.01). Furthermore, a greater number of H. pylori was associated with a stronger expression of HLA-DR antigens (P < 0.001). We conclude that H. pylori is indirectly related to HLA-DR expression on gastric epithelium. H. pylori is the first microbial agent that has been suggested to be associated with epithelial HLA-DR expression in the human gastrointestinal tract.

Class II antigen expression on gastric epithelium was investigated using an immunoperoxidase method in relation to the degree of inflammatory cell infiltration in the lamina propria. Sixty-six biopsy specimens from 43 patients with chronic gastritis were examined. The frequency of HLA-DR expression in specimens with cell infiltration was 94%, while that in specimens without cell infiltration was 24%. There was significant difference in the frequency of HLA-DR expression between the two groups (P less than 0.01). HLA-DR was most intensely expressed in the glandular neck portion. The frequency and extent of class II antigen expression on gastric epithelium with cell infiltration were in the following order: DR greater than DP greater than DQ. The extent of DR and DP, but not DQ expression generally paralleled the degree of cell infiltration. Intestinal metaplasia was found in 13 specimens. In the area of intestinal metaplasia, epithelial class II staining was absent except for one specimen. These results suggest that the respective genes of three class II antigens are regulated by different mechanisms and that an immunological mechanism plays a role in the pathogenesis of gastritis.