Function of Eosinophils from Eosinophilic pneumonia : Purification and Analysis of Tcell-derived eosinophil chemotactic factor

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Although we couldn't success the finding of structure of eosinophil chemotactic factor derived from T-cell, we could get an interesting result during this time. We assessed the expression of galectin-9 with immunostaining and in situ hybridization both in the lesion of angiolymphoid hyperplasia with eosinophilia, and peripheral blood eosinophils of eosinophilic patients (E-Eos) in comparison with those of normal volunteers (N-Eos). Regulation of expression of galectin-9 on eosinophils and the effect of galectin-9 on apoptosis of eosinophil were also evaluated. Many eosinophils infiltrating the site were positive for galectin-9. Surface and intracellular immunoreactive galectin-9 was more evident in E-Eos than N-Eos. When eosinophils were cultured with IL-5 in vitro, the surface galectin-9 expression of E-Eos was significantly, down-regulated, although that of N-Eos was not affected. Treatment of eosinophils with dexarnethasone or anti-Fas antibody significantly up-regulated the surface galectin-9 expression of E-Eos. In contrast, dexamethasone controversially down-regulated the surface galectin-9 of N-Eos, although anti-Fas antibody failed to affect on the surface galectin-9 expression. We also found that recombinant galectin-9 significantly suppressed apoptosis of E-Eos, whereas it apparently enhanced apoptosis of N-Eos. Furthermore, dexamethasone-induced apoptosis of N-Eos was significantly suppressed by galectin-9, whereas galectin-9 failed to induce significant change in dexamethasoneinduced apoptosis of E-Eos. In contrast, apoptosis induced by anti-Fas antibody in both N-Eos and E-Eos was enhanced by galectin-9. These findings suggested that galectin-9 was produced by eosinophils, and galectin-9 showed heterogeneous effects and kinetics to eosinophils, and this factor might be one of crucial factors in eosinophilic inflammation.