title: TLR2-dependent amelioration of allergic airway inflammation by parasitic nematode type II MIF in mice.
abstract: In our previous studies, the recombinant type II macrophage migration inhibitory factor homologue (rAs-MIF) secreted from Anisakis simplex suppressed experimental inflammation mouse model through IL-10 production and CD4(+)CD25(+)Foxp3(+) T-cell recruitment. Also, TLR2 gene expression was significantly increased following rAs-MIF treatment. To know the relation between TLR2 and amelioration mechanisms of rAs-MIF, we induced allergic airway inflammation by ovalbumin and alum with or without rAs-MIF under TLR2 blocking systems [anti-TLR2-specific antibody (α-mTLR2 Ab) treatment and using TLR2 knockout mice]. As a result, the amelioration effects of rAs-MIF in allergic airway inflammation model (diminished inflammation and Th2 response in the lung, increased IL-10 secretion, CD4(+)CD25(+)Foxp3(+) T-cell recruitment) were diminished under two of the TLR2 blocking model. The expression of TLR2 on the surface of lung epithelial cell was significantly elevated by rAs-MIF treatment or Pam3CSK (TLR2-specific agonist) treatment, but they might have some competition effect on the elevation of TLR2 expression. In addition, the elevation of IL-10 gene expression by rAs-MIF treatment was significantly inhibited by α-mTLR2 Ab or Pam3CSK pretreatment. In conclusion, anti-inflammatory effects of the rAs-MIF on OVA-induced allergic airway inflammation might be closely related to TLR2.
authors.affiliation: Department of Parasitology, School of Medicine, Pusan National University, Yangsan-si, Korea.
authors.forename: M K
authors.initials: MK
authors.lastname: Cho
authors.forename: M K
authors.initials: MK
authors.lastname: Park
authors.forename: S A
authors.initials: SA
authors.lastname: Kang
authors.forename: S K
authors.initials: SK
authors.lastname: Park
authors.forename: J H
authors.initials: JH
authors.lastname: Lyu
authors.forename: D-H
authors.initials: DH
authors.lastname: Kim
authors.forename: H-K
authors.initials: HK
authors.lastname: Park
authors.forename: H S
authors.initials: HS
authors.lastname: Yu
mesh_terms: D000534:Alum Compounds; D000818:Animals; D017163:Anisakis; D004195:Disease Models, Animal; D005260:Female; D015801:Helminth Proteins / Q000276:immunology*; D006967:Hypersensitivity / Q000276:immunology* / Q000473:pathology; D007249:Inflammation / Q000139:chemically induced / Q000276:immunology; D016753:Interleukin-10 / Q000276:immunology; D008168:Lung / Q000276:immunology; D008263:Macrophage Migration-Inhibitory Factors / Q000276:immunology*; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D010047:Ovalbumin; D006377:T-Lymphocytes, Helper-Inducer / Q000276:immunology; D050378:T-Lymphocytes, Regulatory / Q000276:immunology; D051195:Toll-Like Receptor 2 / Q000235:genetics / Q000276:immunology*
chemical_list: D000534:Alum Compounds; D015801:Helminth Proteins; D008263:Macrophage Migration-Inhibitory Factors; C493486:Tlr2 protein, mouse; D051195:Toll-Like Receptor 2; D016753:Interleukin-10; C041524:aluminum sulfate; D010047:Ovalbumin
keywords: CD4+CD25+Foxp3+T cell; allergic airway inflammation; rAs-MIF; toll-like receptor 2