2001 Fiscal Year Final Research Report Summary
Function of Eosinophils from Eosinophilic pneumonia : Purification and Analysis of Tcell-derived eosinophil chemotactic factor
| Project/Area Number |
11670584
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | Kumamoto University |
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Principal Investigator |
SAITA Naoki Kumamoto U, University Hospital, Assistant Professor, 医学部・附属病院, 助手 (10274698)
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| Project Period (FY) |
1999 – 2001
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| Keywords | Eosimophilic patients / Apoptosis / galectin 9 |
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| Research Abstract |
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.
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[Publications] Naoki Saita, Eisuke Goto, Taro Yamamoto, Kaori Tsumori, Hirotsugu Kohrogi, Keishi Maruo, Motohiro Takeya, Tomomichi Ono, Yumiko Kashio, Kazuhiro Nakamura, Mitsuomi Hirashima: "Association of Galectin-9 with Eosinophil Apoptosis"Int Arch Allergy Immunol. (in press).
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