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SUMMARY.The in-vitro adhesion of Vibrio cholerae to intestinal mucous membrane was studied in isolated adult-rabbit ileal loops. Antisomatic antiserum against V . cholerae Inaba could inhibit adhesion of three different strains of V. cholerae Inaba but had no effect on the adhesion of two different strains of enterotoxigenic NAG vibrios. The antiserum's bacterial agglutinin titre was 320, its anti-Inaba lipopolysaccharide (LPS) titre was 16 000 and its anti-flagellar antibody titre was 3200. Conversely, anti-live V. cholerae Inaba antiserum absorbed with boiled cells of Inaba and devoid of antisomatic antibody, could not inhibit adhesion of the same three strains of V. cholerae Inaba. This antiserum had no anti-LPS or bacterial agglutinin activity, but its anti-flagellar antibody titre was 32 000. Thus, ability to inhibit adhesion of V. cholerae could be correlated only with antisomatic (anti-LPS) antibody activity. Antisomatic antiserum had no activity against 'adhesin', a V. cholerae surface antigen described by Freter. Conversely anti-live V. cholerae antiserum absorbed with boiled cells showed anti-adhesin activity even at a dilution of 1 in 200. LPS preparations from V. cholerae strain 569B Inaba could inhibit adhesion of two different Inaba strains to the intestinal mucous membrane. It is concluded that the somatic antigen plays a major role in the adhesion of V. cholerae to the intestinal mucous membrane.

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SUMMARY.In studies with the adult-rabbit ileal-loop model, antibodies to the lipopolysaccharide somatic-antigen component of Vibrio cholerae gave passive protection against challenge with live V . cholerae. The antisomatic antibodies had no effect on bacterial proliferation and toxin production either in vitlo or in vitro; after challenge, antibody-protected and non-protected rabbit ileal loops developed almost identical amounts of cholera toxin and numbers of V. cholerae. The protection could be correlated only with a 10-1 5-fold reduction in the number of V. cholerae adherent to the mucous membrane of the antibody-protected loops. The amount of cholera toxin in the two sets of loops ranged from 1600 to 3200 units. In contrast, when biologically active cholera toxin was prepared in vitro, the amount required to induce ileal-loop secretion was very large (25 600 units). These findings indicate that toxin production by adherent vibrios on the surface of the mucous membrane is an important factor in the pathogenesis of cholera.

SUMMARYTbe route of immunization was observed to play a significant role in deciding the outcome of immunization with killed mycobacterial vaccines. Wbereas the slow growers were immunogenic by both intraperitoneal and intradermal routes, the rapid growers were immunogenic only by intradcrmal route. The non-rcsponder state of miee to Mycobacterium vaccae by i.p. route of immunization eould be corrected by prior treatment with poly I: poly C, an interferon inducer, or indomethacin, a prostaglandin inhibitor. Antigen-presenting efficiency of peritoneal and spleen cells were compared employing M. vaccae and M. tuberculosis H37Rv primed T cells and corresponding sonicates as antigens in an in vitro lymphoeyte transformation test. Irradiated spleen eells presented both the antigens efficiently. However, with peritoneal cells as antigen-presenting cells, proliferative response against only M. tubercutosis was observed; proliferation of M. vaccae primed T cells was very poor. Peritoneal cells of poly I:poly C treated mice showed distinct improvement in their efficiency of presentation; even para formaldehyde-fixed peritoneal cells gave an efficient stimulation with M. vaccae. The percentage of la-positive fraction in peritoneal cells was very low (5-95%) in comparison with spleen cells (38-37'^n). Poly I: poly C treatment resulted in increase in tbe la-positive cell fraction ofthe peritonea! cells to 24-5"';i.