Author/Authors :
Komiya، نويسنده , , Akiko and Nagase، نويسنده , , Hiroyuki and Yamada، نويسنده , , Hirokazu and Sekiya، نويسنده , , Takashi and Yamaguchi، نويسنده , , Masao and Sano، نويسنده , , Yasuyuki and Hanai، نويسنده , , Nobuo and Furuya، نويسنده , , Akiko and Ohta، نويسنده , , Ken and Matsushima، نويسنده , , Kouji and Yoshie، نويسنده , , Osamu and Yamamoto، نويسنده , , Kazuhiko and Hirai، نويسنده , , Koichi، نويسنده ,
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-γ 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.
Keywords :
asthma , CCR3 , chemokines , eosinophils , Glucocorticoids