TLR 2‐dependent amelioration of allergic airway inflammation by parasitic nematode type II MIF in mice

Abstract

Summary: In our previous studies, the recombinant type II macrophage migration inhibitory factor homologue (r A s‐MIF) secreted from A nisakis simplex suppressed experimental inflammation mouse model through IL‐10 production and CD 4+CD 25+F oxp3+ T‐cell recruitment. Also, TLR 2 gene expression was significantly increased following r A s‐MIF treatment. To know the relation between TLR 2 and amelioration mechanisms of r A s‐MIF, we induced allergic airway inflammation by ovalbumin and alum with or without r A s‐MIF under TLR 2 blocking systems [anti‐TLR 2‐specific antibody (α‐m TLR 2 Ab) treatment and using TLR 2 knockout mice]. As a result, the amelioration effects of r A s‐MIF in allergic airway inflammation model (diminished inflammation and T h2 response in the lung, increased IL‐10 secretion, CD 4+CD 25+F oxp3+ T‐cell recruitment) were diminished under two of the TLR 2 blocking model. The expression of TLR 2 on the surface of lung epithelial cell was significantly elevated by r A s‐MIF treatment or P am3 CSK (TLR 2‐specific agonist) treatment, but they might have some competition effect on the elevation of TLR 2 expression. In addition, the elevation of IL‐10 gene expression by r A s‐MIF treatment was significantly inhibited by α‐m TLR 2 Ab or P am3 CSK pretreatment. In conclusion, anti‐inflammatory effects of the r A s‐MIF on OVA‐induced allergic airway inflammation might be closely related to TLR 2.