title: Possible regulatory role of galectin-9 on Ascaris suum-induced eosinophilic lung inflammation in mice.
abstract: BACKGROUND
  Galectin-9 (Gal-9) is a member of the galectin family of lectins that exhibit binding affinity for β-galactosides. We found a T cell line-derived Gal-9 with novel eosinophil chemoattractant activity, but its role in eosinophilic inflammation of the lung is unknown. We evaluated the role of Gal-9 in Ascaris suum-induced eosinophilic lung inflammation in mice.
  
  
  METHODS
  To evaluate the role of Gal-9 in Ascaris suum-induced eosinophilic lung inflammation, we developed a mouse model of eosinophilic pneumonia induced by the Ascaris suum antigen, and analyzed eosinophilic inflammation in Gal-9-deficient mice. The therapeutic effects of recombinant Gal-9 on lung inflammation were also examined in this mouse model. To evaluate lung inflammation, numbers of inflammatory cells and cytokine levels in the bronchoalveolar lavage fluid (BALF) were estimated by flow cytometry and enzyme-linked immunosorbent assay, respectively.
  
  
  RESULTS
  The BALF of this mouse model of eosinophilic pneumonia induced by the Ascaris suum antigen contained increased numbers of inflammatory cells and elevated Gal-9 levels. Compared with wild-type mice, the BALF of Gal-9-deficient mice contained higher numbers of both eosinophils and T helper type 2 (Th2) cells. Th2 cytokines and eotaxin levels were also higher, and levels of CD4+CD25+Foxp3+ regulatory T cells were lower in Gal-9-deficient mice than in wild-type mice. Intranasal administration of recombinant Gal-9 prevented eosinophilic inflammation of the lung and upregulated the release of endogenous Gal-9.
  
  
  CONCLUSIONS
  Our findings suggest that Gal-9 negatively regulates Th2-mediated eosinophilic inflammation of the lung and that Foxp3+ regulatory T cells might be involved in suppressing allergic inflammation.
authors.affiliation: Department of Respiratory Medicine, Kawasaki Medical School, Okayama, Japan. kshigeki@med.kawasaki-m.ac.jp
authors.forename: Shigeki
authors.initials: S
authors.lastname: Katoh
authors.forename: Souichi
authors.initials: S
authors.lastname: Oomizu
authors.forename: Toshiro
authors.initials: T
authors.lastname: Niki
authors.forename: Hiroki
authors.initials: H
authors.lastname: Shimizu
authors.forename: Yasushi
authors.initials: Y
authors.lastname: Obase
authors.forename: Masataka
authors.initials: M
authors.lastname: Korenaga
authors.forename: Mikio
authors.initials: M
authors.lastname: Oka
authors.forename: Mistuomi
authors.initials: M
authors.lastname: Hirashima
mesh_terms: D000818:Animals; D000947:Antigens, Helminth / Q000276:immunology*; D017165:Ascaris suum / Q000276:immunology*; D001992:Bronchoalveolar Lavage Fluid / Q000166:cytology / Q000276:immunology; D016207:Cytokines / Q000276:immunology; D004195:Disease Models, Animal; D004802:Eosinophilia / Q000188:drug therapy / Q000276:immunology*; D005260:Female; D037161:Galectins / Q000235:genetics / Q000276:immunology* / Q000627:therapeutic use; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D011014:Pneumonia / Q000188:drug therapy / Q000276:immunology*; D011994:Recombinant Proteins / Q000627:therapeutic use; D050378:T-Lymphocytes, Regulatory / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology
chemical_list: D000947:Antigens, Helminth; D016207:Cytokines; D037161:Galectins; D011994:Recombinant Proteins; C508186:galectin 9, mouse