Relative significance of mannose-sensitive hemagglutinin and toxin-coregulated pili in colonization of infant mice by Vibrio cholerae El Tor.
AUTOR(ES)
Attridge, S R
RESUMO
A previously described in-frame deletion in mshA--the gene encoding the structural subunit of the mannose-sensitive hemagglutinin pilus--has been introduced into the chromosome of three El Tor O1 strains of Vibrio cholerae. None of the deltamshA mutants showed significant attenuation or loss of colonization potential in the infant mouse cholera model. A second mutation, created by insertion of a kanamycin resistance cartridge into deltamshA, also failed to affect in vivo behavior. In contrast, strains carrying mutations in tcpA (encoding the monomer of the toxin-coregulated pilus [TCP]) were markedly attenuated and showed dramatically impaired colonization. This result was in line with those of previous studies. Protection tests performed with antibodies to TCP and to MshA showed that only the former were able to confer immunity against El Tor O1 challenge in this model. Studies with mutants constructed from two O139 strains similarly suggest that TCP but not mannose-sensitive hemagglutinin pili are critical for colonization by strains of this serogroup.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=174231Documentos Relacionados
- Toxin-coregulated pilus, but not mannose-sensitive hemagglutinin, is required for colonization by Vibrio cholerae O1 El Tor biotype and O139 strains.
- Investigation of the Roles of Toxin-Coregulated Pili and Mannose-Sensitive Hemagglutinin Pili in the Pathogenesis of Vibrio cholerae O139 Infection
- A Role for the Mannose-Sensitive Hemagglutinin in Biofilm Formation by Vibrio cholerae El Tor
- Role for Mannose-Sensitive Hemagglutinin in Promoting Interactions between Vibrio cholerae El Tor and Mussel Hemolymph
- Analysis of expression of toxin-coregulated pili in classical and El Tor Vibrio cholerae O1 in vitro and in vivo.