| Literature DB >> 14698143 |
Akiko Komiya1, Hiroyuki Nagase, Hirokazu Yamada, Takashi Sekiya, Masao Yamaguchi, Yasuyuki Sano, Nobuo Hanai, Akiko Furuya, Ken Ohta, Kouji Matsushima, Osamu Yoshie, Kazuhiko Yamamoto, Koichi Hirai.
Abstract
Eotaxin-1/CCL11, eotaxin-2/CCL24, and eotaxin-3/CCL26 bind specifically and exclusively to CC chemokine receptor (CCR) 3, which is a potential therapeutic target in treating the peribronchial eosinophilia associated with allergic airway diseases. Bronchial epithelial cells represent an important source of chemokines, and thus we investigated in vitro and in vivo expression of eotaxin-2 and eotaxin-3 in bronchial epithelial cells in comparison with that of eotaxin-1. Immunohistochemistry showed increased expression of both eotaxin-2 and eotaxin-3 in addition to eotaxin-1 in asthmatics. Considerable amounts of eotaxins were secreted by bronchial epithelial lineage. As with eotaxin-1 production, generation of eotaxin-2 and eotaxin-3 by bronchial epithelial cells was up-regulated by IL-4 and IL-13, and attenuated by IFN-gamma and glucocorticoids. In addition to eotaxin-1 expression, but also eotaxin-2 and eotaxin-3 expression in the bronchial epithelium should be taken into consideration when developing the therapeutic strategies to treat eosinophilic airway diseases.Entities:
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Year: 2003 PMID： 14698143 DOI： 10.1016/j.cellimm.2003.10.001
Source DB: PubMed Journal: Cell Immunol ISSN： 0008-8749 Impact factor: 4.868