Previously, we have shown that the Vibrio cholerae haemagglutinin/protease (HA/P) accounts for significant remaining toxicity of CVD110, an attenuated V. cholerae 01 El Tor live oral vaccine-strain. The present report demonstrates that endogenous nitric oxide (NO) production modulates HA/P-mediated cytotoxicity in Madin-Darby canine kidney cell strain I (MDCK-I) epithelial cells. The basal levels of endogenous NO suppressed the cytotoxicity of HA/P, whereas inhibition of NO production with nitro-L-arginine methyl-ester (L-NAME) made the MDCK-I cells susceptible even to low concentrations of the cytotoxin. The inhibition of NO production caused a reinforcement of the HA/P- mediated distortion of a tight junction-associated protein ZO-1 and increment of filamentous actin at the apical and the lateral membrane domains. The mechanism by which NO exerts its modulatory action is not likely to be from its direct interaction with the zinc-containing catalytic domain of HA/P, since two NO donors, sodium nitroprusside (SNP) and S-nitroso-N-acetyl-D, L-penicillamine (SNAP), did not affect the proteolytic activity of HA/P. In conclusion, the endogenous NO in the MDCK-I cells has a modulating effect on the cytotoxicity of HA/P and thus protects the cells against the cytotoxin.

01 Jun 1996·Infection and ImmunityQ2 · MEDICINE

New evidence for an inflammatory component in diarrhea caused by selected new, live attenuated cholera vaccines and by El Tor and Q139 Vibrio cholerae

Q2 · MEDICINE

Article

Author: Edelman, R ; Guerrant, R ; Steiner, T S ; Silva, T M ; Tacket, C O ; Kaper, J B ; Schleupner, M A

Using a lactoferrin latex agglutination assay, we have compared the inflammatory responses to a cholera vaccine candidate, CVD 110, in which all known toxin genes have been deleted or mutated yet still produced significant diarrhea, with a less reactive vaccine strain and wild-type El Tor and 0139 Vibrio cholerae strains. Data suggest that diarrhea due to attenuated and wild-type El Tor V. cholerae, and to a lesser extent 0139 V. cholerae, involves an inflammatory response. Further study is required to further elucidate the mechanism of the process(es) involved.

01 Jan 1994·VaccineQ3 · MEDICINE

Kinetics of the vibriocidal antibody response to live oral cholera vaccines

Q3 · MEDICINE

Article

Author: Carol O. Tacket ; Steven S. Wasserman ; Elizabeth Castañeda ; Myron M. Levine ; Fernando Noriega ; Genevieve A. Losonsky

The best correlate of protection against cholera is the level of serum vibriocidal antibodies, which are primarily directed against the O antigen of Vibrio cholerae O1 and lyse V. cholerae in the presence of complement. We established the timing of peak vibriocidal antibody response using sera from safety/immunogenicity studies of live oral cholera vaccines CVD 103-HgR, CVD 103-HgR2 and CVD 110 among immunologically naive North Americans and Colombians. The serum reciprocal vibriocidal antibody titre was consistently higher 10 days postimmunization than on either day 7 or day 14. This study suggests that recent phase 2 studies of CVD 103-HgR may have underestimated the peak vibriocidal titre by collecting serum on days 7-8 rather than on day 10; future studies of live oral cholera vaccines should take these results into account to obtain the best measurement of peak immunological responses. Because of the rapid drop in vibriocidal antibody titres about 2 weeks after immunization, care must be exercised in comparing immunogenicity of different vaccine candidates, formulations, dosage levels and immunization schedules.

100 Deals associated with Cholera vaccine CVD 110(BruCells NV)

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Indication	Highest Phase	Country/Location	Organization	Date
Cholera	Phase 1	-	BruCells NV	-
Cholera	Phase 1	CH	Berna Biotech AG	-

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