Premium
Amelioration of intestinal colitis by macrophage migration inhibitory factor isolated from intestinal parasites through Toll‐like receptor 2
Author(s) -
CHO M. K.,
LEE C. H.,
YU H. S.
Publication year - 2011
Publication title -
parasite immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.795
H-Index - 75
eISSN - 1365-3024
pISSN - 0141-9838
DOI - 10.1111/j.1365-3024.2010.01276.x
Subject(s) - macrophage migration inhibitory factor , foxp3 , immunology , mesenteric lymph nodes , biology , immune system , inflammation , receptor , tlr2 , medicine , cytokine , innate immune system
Summary In a previous study, we cloned type II MIFs (As‐MIF) from Anisakis simplex 3rd stage larva and expressed a recombinant protein that suppressed allergic airway inflammation via regulatory T (CD4 + CD25 + Foxp3 + T; T reg )‐cell recruitment. In this study, in an effort to evaluate the function of rAs‐MIF on another immune disease, we induced intestinal inflammation in mice using dextran sodium sulphate (DSS) with or without the application of rAs‐MIF treatment to the mice. As a consequence, weight losses were recovered, and the value of disease activity index (DAI) was reduced by rAs‐MIF treatment during the experimental period. The levels of TGF‐β and IL‐10 in the spleens and mesenteric lymph nodes (MLN) from the rAs‐MIF‐treated mice were higher, but the levels of IFN‐γ, IL‐6 and IL‐13 were lower than those of the mice treated with DSS but not with rAs‐MIF. Additionally, the T reg cells observed were greatly increased in the MLNs of the rAs‐MIF‐treated mice than those of mice not treated with rAs‐MIF. The results of our in vitro experiments showed that the elevated IL‐10 production induced by rAs‐MIF was generated via toll‐like receptor 2. In conclusion, rAs‐MIF appears to ameliorate DSS‐induced colitis and may prove useful as a therapeutic agent for the treatment of intestinal inflammatory disease.