Anti-Blood Group Lewis X monoclonal antibody, clone R24

Background and aims: We tested if host gastric Lewis antigens and the babA2 genotype of Helicobacter pylori correlated with clinicohistological outcome. Methods: We enrolled 188 dyspeptic patients ( 45 with duodenal ulcer, 45 with gastric ulcer, and 98 with chronic gastritis) with H pylori infection, proved by culture and gastric histology, reviewed by the updated Sydney system. Gastric expression of Lewis (Le) antigens Le(a), Le(b), Le(x), and Le(y) was determined immunochemically to determine intensity ( range 0 - 3). The corresponding 188 H pylori isolates were screened for babA2 genotype by polymerase chain reaction. Results: All H pylori isolates had a positive babA2 genotype. We identified Le(a) in 33.5%, Le(b) in 72.9%, Le(x) in 86.2%, and Le(y) in 97.4% of biopsies from these 188 patients. Patients who expressed Le(b) had a higher H pylori density than those who did not express Le(b) ( p< 0.001). Among 139 patients who expressed Le(b), H pylori density increased with a higher Le(b) intensity ( p< 0.05). Gastric atrophy decreased with Le(b) intensity and thus resulted in lower H pylori density in the antrum ( p< 0.05). For the 49 patients without gastric Leb expression, H pylori density was positively related with Le(x) and Le(a) expression ( p< 0.05). Conclusions: Taiwanese H pylori isolates are 100% babA2 genopositive. Gastric Le(b) as well as Le(x) intensity may be major determinants of H pylori density. While lacking gastric Le(b) expression, Le(x) and Le(a) were closely related to H pylori colonisation.

Recent studies have demonstrated that selectins, a new family of cell-adhesion molecules with similar domain structures, mediate the adhesion of peripheral blood cells to interleukin-1 (IL-1)-activated endothelium. In the present study the authors evaluated the role of E-selectin-Sialyl Lewis x (SLe(x))/ Sialyl Lewis a (SLe(a)) interaction in mediating in vitro adhesion of two colon cancer cell lines, HT-29 and COLO 201, to human umbilical cord endothelial cells (HUVEC). Colon cancer cell lines had a strong expression of blood group-related carbohydrate epitopes as evaluated by fluorescence-activated cell sorter (FAGS) analysis. It was established that adhesion of HT-29 and COLO 201 cells to IL-1 stimulated HUVEC was calcium dependent and could be inhibited by a monoclonal antibody directed against E-selectin. Prior incubation of cells with two different antibodies directed against SLe(x) and antibodies directed against related Lewis epitopes, Le(x) and Le(a), had no significant effect on adhesion. Three antibodies directed against SLe(a) differed in their capacity to inhibit the adhesion of HT-29 and COLO 201 cells to HUVEC. Only one antibody directed against the SLe(a) structure was effective in inhibiting adhesion of both COLO 201 and HT-29 cells. The difference could not be attributed to titre, the type or number of glycoproteins, or to a difference in the amount of SLe(a) present on individual proteins, suggesting that presence and right presentation of SLe(a) epitope might be important for adhesion of colon cancer cells. Finally, in the in vitro system used, adhesion of HT-29 and COLO 201 cells to activated HUVEC is mediated predominantly by E-selectin/SLe(a) interaction. SLe(x) and related epitopes, Le(x) and Le(a), seem to have limited relevance for colon cancer cell recognition of E-selectin.