• Hitomi Yamamoto, Yumiko Kashio, Hiroki Shoji, Rika Shinonaga, Teizo Yoshimura, Nozomu Nishi, Takeshi Nabe, Takanori Nakamura, Shigekatsu Kohno, and Mitsuomi Hirashima.
• Department of Immunology and Immunopathology, Kagawa University Faculty of Medicine, Kita-Gun, Kagawa, Japan.
• Int. Arch. Allergy Immunol. 2007 Jan 1; 143 Suppl 1: 95-105.

BackgroundThere 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.MethodsAirway 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.ResultsIn 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).ConclusionsThe present results provide evidence that Gal-9 is not involved in airway hypersensitivity, but is partly involved in prolonged eosinophil accumulation in the lung.

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