K. Walia et al., Spectrum of gut immunologic reactions: Selective induction of distinct responses to Vibrio cholerae WO7 and its toxin, MICROB IMMU, 44(11), 2000, pp. 931-940
Past studies with Vibrio cholerae have shown that cholera toxin (CT) is mai
nly responsible for inducing T helper type 2 (Th2) responses with systemic
IgG1, IgE and mucosal secretory IgA (sIgA) antibodies. In this study, V. ch
olerae WO7, which produces novel toxin unrelated to CT, was given orally to
mice in order to determine whether the strain V. cholerae WO7 differs from
V. cholerae 569B, which produces CT, in the nature of responses generated
at the gut and splenic level. The analysis of immune responses evoked by V.
cholerae WO7 in the gut of mice revealed striking differences as compared
to those elicited by V. cholerae 569B infection. To assess the T helper cel
l type responses, lymphocytes from Peyer's patches and the spleen were stim
ulated in vitro for studying the cytokine patterns. PP and SP lymphoid cell
s from V. cholerae WO7 infected animals elaborated significant amounts of I
L-2, IFN-gamma 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 a
nd IL-10 with traces of IFN-gamma, On the other hand, infection with V. cho
lerae 569B yielded mainly Th2 type responses at Peyer's patches as well as
the splenic level. Infection with both V. cholerae WO7 and 569B induced tox
in-specific IgA secreting cells at the gut and splenic level along with IgG
I secreting cells, indicating that both V. cholerae WO7 and 569B evoke an a
ntigen-specific Th2 type of response in the gut as well as spleen. The pers
istence of IgA along with Th1-type cytokines indicates an alternate inducti
on mechanism since mucosal IgA responses are usually associated with Th2-ty
pe responses. These observations are suggestive of a common mechanism emplo
yed by the host to clear different strains of V. cholerae infection (569B a
nd WO7 in this case), while the nature of toxins elaborated failed to modul
ate the net outcome of the infection caused by V. cholerae.