Spectrum of Gut Immunologic Reactions:Selective Induction of Distinct Responses to Vibrio cholerae WO7 and Its Toxin
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Past studies with <i>Vibrio cholerae</i> have shown that cholera toxin (CT) is mainly responsible for inducing T helper type 2 (Th2) responses with systemic IgG1, IgE and mucosal secretory IgA (sIgA) antibodies. In this study, <i>V. cholerae</i> WO7, which produces novel toxin unrelated to CT, was given orally to mice in order to determine whether the strain <i>V. cholerae</i> WO7 differs from <i>V. cholerae</i> 569B, which produces CT, in the nature of responses generated at the gut and splenic level. The analysis of immune responses evoked by <i>V. cholerae</i> WO7 in the gut of mice revealed striking differences as compared to those elicited by <i>V. cholerae</i> 569B infection. To assess the T helper cell type responses, lymphocytes from Peyer's patches and the spleen were stimulated <i>in vitro</i> for studying the cytokine patterns. PP and SP lymphoid cells from <i>V. cholerae</i> WO7 infected animals elaborated significant amounts of IL-2, IFN-γ and IL-12 by 7 days p.i., suggesting a Th1 type of response. However by 15 days p.i., the PP and SP lymphoid cells secreted only IL-6 and IL-10 with traces of IFN-γ. On the other hand, infection with <i>V. cholerae</i> 569B yielded mainly Th2 type responses at Peyer's patches as well as the splenic level. Infection with both <i>V. cholerae</i> WO7 and 569B induced toxin-specific IgA secreting cells at the gut and splenic level along with IgG1 secreting cells, indicating that both <i>V. cholerae</i> WO7 and 569B evoke an antigen-specific Th2 type of response in the gut as well as spleen. The persistence of IgA along with Th1-type cytokines indicates an alternate induction mechanism since mucosal IgA responses are usually associated with Th2-type responses. These observations are suggestive of a common mechanism employed by the host to clear different strains of <i>V. cholerae</i> infection (569B and WO7 in this case), while the nature of toxins elaborated failed to modulate the net outcome of the infection caused by <i>V. cholerae</i>.
- Japanese Journal of Microbiology
Japanese Journal of Microbiology 44(11), 931-940, 2000-11-20
Center For Academic Publications Japan