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Systemic delivery of a crude extract of the tapeworm, Hymenolepis diminuta , exerts an anti‐inflammatory effect in a murine model of colitis
Author(s) -
Wang Arthur,
McKay Derek
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.852.16
Subject(s) - hymenolepis diminuta , colitis , myeloperoxidase , inflammatory bowel disease , immune system , pharmacology , immunology , tumor necrosis factor alpha , chemistry , splenocyte , inflammation , biology , medicine , disease , helminths , cestoda
Awareness of how parasites diminish the host's immune response would, in theory, allow for the development of new therapies to combat autoimmune and inflammatory disease. In an in vitro analysis, we showed that a >50kDa fraction from adult Hymenolepis diminuta blocked mitogen‐induced T cell activation. Here, we tested the hypothesis that this H. diminuta extract would block the colitis that develops in mice in response to intra‐rectal instillation of dinitrobenzene sulphonic acid (DNBS) – a system used as a model of the human inflammatory bowel disease, Crohn's disease. Balb/c mice were treated with 100μl of 50% ethanol ir (control), 3mg of DNBS (in ethanol, ir) or DNBS + worm antigen (3×1mg ip injections over 3 days). Mice were sacrificed 72h after DNBS and clinical disease scores, histological damage scores, colonic myeloperoxidase (MPO, indicates granulocyte infiltration) activity, and TNFα and IL‐10 production by splenocytes assessed. DNBS treatment caused colitis as shown by wasting, elevated MPO (14.0±3.9 vs. 2.0±0.3 U/mg; n=3) and the production of TNFα (783±27 pg/ml) but not IL‐10. In contrast, mice treated with DNBS + worm antigen showed no mortality and only minor signs of colitic disease that was accompanied by increased IL‐10 (2.0±0.9 ng/ml; n=3). Purification and synthesis of this immunosuppressive factor from H. diminuta could be used to treat inflammatory diseases. CCFC funded.