title: Involvement of galectin-9 in guinea pig allergic airway inflammation.
abstract: BACKGROUND
  There is little information about the involvement of galectin-9 (Gal-9) in allergic inflammation. Thus, we investigated the role of Gal-9 in asthma model guinea pigs.
  
  
  METHODS
  Airway resistance (R(aw)) was measured using a double-flow plethysmograph system. Gal-9 expression in the lung was assessed by Western blot and immunohistochemistry. Eosinophil chemotactic activity was evaluated in a chamber containing a polyvinylpyrolidone-free membrane. Cell apoptosis was analyzed on a flowcytometry with propidium iodide.
  
  
  RESULTS
  In cloning guinea pig Gal-9 we identified three isoforms that differ only in the length of their linker peptides, just as with human Gal-9. Guinea pig Gal-9 was found to be a chemoattractant for eosinophils and to promote induction of apoptosis in sensitized but not non-sensitized T lymphocytes. In allergic airway hypersensitivity model, a low level of Gal-9 expression was observed in the nonsensitized/nonchallenged group, but upregulation was detected at 7 h after challenge and sustained up to 24 h. Such upregulation correlated with elevation of eosinophil peroxidase activity but not with increased R(aw).
  
  
  CONCLUSIONS
  The present results provide evidence that Gal-9 is not involved in airway hypersensitivity, but is partly involved in prolonged eosinophil accumulation in the lung.
authors.affiliation: Department of Immunology and Immunopathology, Kagawa University Faculty of Medicine, Kita-Gun, Kagawa, Japan.
authors.forename: Hitomi
authors.initials: H
authors.lastname: Yamamoto
authors.forename: Yumiko
authors.initials: Y
authors.lastname: Kashio
authors.forename: Hiroki
authors.initials: H
authors.lastname: Shoji
authors.forename: Rika
authors.initials: R
authors.lastname: Shinonaga
authors.forename: Teizo
authors.initials: T
authors.lastname: Yoshimura
authors.forename: Nozomu
authors.initials: N
authors.lastname: Nishi
authors.forename: Takeshi
authors.initials: T
authors.lastname: Nabe
authors.forename: Takanori
authors.initials: T
authors.lastname: Nakamura
authors.forename: Shigekatsu
authors.initials: S
authors.lastname: Kohno
authors.forename: Mitsuomi
authors.initials: M
authors.lastname: Hirashima
mesh_terms: D000403:Airway Resistance / Q000502:physiology*; D017398:Alternative Splicing; D000595:Amino Acid Sequence; D000818:Animals; D017209:Apoptosis; D001249:Asthma / Q000209:etiology / Q000503:physiopathology; D001483:Base Sequence; D001992:Bronchoalveolar Lavage Fluid / Q000166:cytology; D015496:CD4-Positive T-Lymphocytes / Q000378:metabolism; D002634:Chemotaxis, Leukocyte; D018076:DNA, Complementary / Q000235:genetics; D004195:Disease Models, Animal; D047209:Eosinophil Peroxidase / Q000032:analysis; D004804:Eosinophils / Q000166:cytology / Q000502:physiology*; D005091:Exons / Q000235:genetics; D037161:Galectins / Q000096:biosynthesis / Q000737:chemistry / Q000235:genetics / Q000302:isolation & purification / Q000502:physiology*; D006168:Guinea Pigs; D006801:Humans; D007114:Immunization; D008168:Lung / Q000737:chemistry / Q000473:pathology; D008297:Male; D008969:Molecular Sequence Data; D016366:Open Reading Frames / Q000235:genetics; D010047:Ovalbumin / Q000633:toxicity; D020033:Protein Isoforms / Q000737:chemistry / Q000235:genetics; D011657:Pulmonary Eosinophilia / Q000473:pathology / Q000503:physiopathology*; D011993:Recombinant Fusion Proteins / Q000302:isolation & purification / Q000502:physiology; D012130:Respiratory Hypersensitivity / Q000209:etiology / Q000503:physiopathology*; D016415:Sequence Alignment; D017386:Sequence Homology, Amino Acid; D013045:Species Specificity
chemical_list: D018076:DNA, Complementary; D037161:Galectins; C105032:LGALS9 protein, human; D020033:Protein Isoforms; D011993:Recombinant Fusion Proteins; C508186:galectin 9, mouse; D010047:Ovalbumin; D047209:Eosinophil Peroxidase