Hymenolepis diminuta is spontaneously expelled from mice; concomitant with worm expulsion was protection against
colitis induced by
dinitrobenzene sulphonic
acid (
DNBS). Here we examined the immune response mobilized by Balb/c and C57Bl/6 male mice in response to H. diminuta and assessed the requirement for CD4+ cells (predominantly T cells) in worm expulsion and the anti-colitic effect. Wild-type (CD4+) or CD4 knock-out (CD4-/-) mice received five H. diminuta cysticercoids and segments of jejunum and mesenteric lymph nodes (MLNs), or spleen, were excised 5, 8 and 1l days later for
mRNA analysis and
cytokine production, respectively. In separate experiments uninfected and infected mice received
DNBS by intra-rectal infusion and indices of
inflammation were assessed 3 days later (i.e. 11 days p.i.).
Infection of Balb/c mice resulted in a time-dependent increase in intestinal
mRNA for Foxp3, a marker of natural regulatory T cells, and markers of alternatively activated macrophages (arginase-1, FIZZ1), while
concanavalin-A activation of MLN cells revealed a significant increase in T helper 2 (TH2) type
cytokines:
IL-4, -5, -9, -10, -13. MLN cells showed a reduced ability to induce Foxp3 expression upon stimulation. CD4-/- mice did not display this response to
infection, but surprisingly did expel H. diminuta. Moreover,
DNBS-induced
colitis in CD4-/- mice (wasting, tissue damage, elevated
myeloperoxidase) was not reduced by H. diminuta
infection, whereas time-matched infected CD4+ C57Bl/6 mice had significantly less
DNBS-induced
inflammation.
IN CONCLUSION: