Vibrio cholerae O1 adherence to villi and lymphoid follicle epithelium: in vitro model using formalin-treated human small intestine and correlation between adherence and cell-associated hemagglutinin levels

Abstract

Formalin-fixed human small intestinal mucosa possessing villi and lymphoid follicle epithelium of Peyer's patches at the mucosal surface was used to test the adherence ability of clinically isolated strains of Vibrio cholerae 01. V. cholerae 01 grown on CFA agar for-3 h at 37°C had various levels of cellular hemagglutinins (HAs) and manifested adherence abilities that were roughly correlated with the cellular HA levels, irrespective of cellular HA types. V. cholerae 01 adhered better to epithelium over ileal lymphoid follicles than to epithelium ofjejunal or ileal villi. Cells of different morphology which constituted lymphoid follicle epithelium were almost equal targets for adherence. In contrast, V. cholerae 01 grown on CFA agar for-20 h at 37C in many cases had lower levels of cellular HAs and adherence abilities. Contrary to the above observations with cellular HAs and adherence, piliation of V. cholerae 01 was rather more extensive at-20 h of incubation at 37°C than at-3 h of incubation at 37°C. L-Fucose inhibited adherence to a varied extent depending on the cellular HA types, while D-mannose enhanced adherence in some strains. Heating of V. cholerae 01 diminished adherence ability. This adherence model system provides a tool by which various V. cholerae 01 strains can be preliminarily tested for adherence ability and site in human small intestine.

Position of human blood group O(H) and phenotype‐determining enzymes in growth and infectious disease

“…107 The adherence of V. cholerae to isolated rabbit brush border membranes, 105 human RBCs, and the lymphoid follicle epithelium of the intestine was (depending on the cellular HA type) inhibited by l-fucose. 108 These observations fit the established concepts. The principle is comprehensively described by Cooling 89 and explained by means of a graphic, according to which the adhesion is thought to be primarily initiated by the pathogen, utilizing preformed fucosylated structures of the host; the adhesion of the Ctx holotoxin occurs via a complex binding process between the five toxin B subunits and the A subunit to cell surface receptors in the small intestine.…”

Adherence to human small intestines of capsulated Vibrio cholerae O139

“…Previously, we demonstrated the in vitro adherence of F. cholerae O1 [12][13][14] to native or formalin-fixed human small intestines including mucus, adsorptive cells and M cells (antigen sampiing cells [15] of ileal Peyer's patch). In this study, we investigated the adherence of capsulated cells of F. cholerae O139 to formalin-fixed and native human small intestines.…”

Proteolytic Activation of Vibrio mimicus (Vm) Major Outer Membrane Protein Haemagglutinin (HA) with Vm‐HA/Protease: Implication for Understanding Bacterial Adherence

“…Colonization of rabbit small intestinal mucosa by clinical and environmental isolates of V. cholerae and V. mimicus was shown (25). Correlation has been established between in vitro adherence to intestinal epithelium of human (26) and rabbit (14) and the cell-associated haemagglutination of V. cholerae. Correlation has also been shown between cell-mediated haemagglutination and the adherence of V. parahaemolyticus to human colonic cell line Caco-2 (18).…”

“…Correlation between the adherence and the cellmediated haemagglutination has been established for many intestinal pathogens (10,18,25,26), and cell surface proteins, such as haemagglutinins (HAs) and/or different types of pili, presumably accomplish both bacterial phenomena (20). In Vibrio cholerae, the etiologic agent of cholera, the toxin-coregulated pilus (TCP) has been documented to be essential for adherence of the classical biotype strains (13); however, the mannosesensitive HA as well as TCP has been implicated in the case of the El Tor strains (21).…”