There is increasing evidence that parasitic helminth
infection has the ability to ameliorate other disease conditions. In this study the ability of the rat tapeworm, Hymenolepis diminuta, to modulate
dinitrobenzene sulfonic acid (
DNBS)-induced
colitis in mice is assessed. Mice receiving
DNBS (3 mg intrarectally) developed
colitis by 72 h
after treatment. Mice infected 8 days before
DNBS with five H. diminuta larvae were significantly protected from the
colitis, as gauged by reduced clinical disease, histological damage scores, and
myeloperoxidase levels. This anticolitic effect was dependent on a viable
infection and helminth rejection, because no benefit was observed in mice given killed larvae or in infected STAT6 knockout mice or rats, neither of which eliminate H. diminuta. The anticolitic effect of H. diminuta was associated with increased colonic
IL-10 mRNA and stimulated splenocytes from H. diminuta- plus
DNBS-treated mice produced more
IL-10 than splenocytes from
DNBS-only treated mice. Coadministration of an anti-IL-10 Ab blocked the anticolitic effect of prophylactic H. diminuta
infection. Also, mice infected 48 h after
DNBS treatment showed an enhanced recovery response. Finally, using a model of OVA
hypersensitivity, we found no evidence of concomitant H. diminuta
infection enhancing enteric responsiveness to subsequent ex vivo OVA challenge. The data show that a viable
infection of H. diminuta in a nonpermissive system exerts a profound anticolitic effect (both prophylactically and as a treatment) that is mediated at least in part via
IL-10 and does not predispose to enhanced sensitivity to bystander
proteins.