Autocrine Regulation of Eotaxin in Normal Human Bronchial Epithelial Cells
Hiroshi Saito, Hisako Shimizu, Kazuo Akiyama
Abstract
Hiroshi Saito, Hisako Shimizu, Kazuo Akiyama
Abstract
Normal human bronchial epithelial cells (NHBECs) spontaneously synthesize and store chemokines including eotaxin, RANTES, or MCP-3. We also observed the constitutive expression of mRNA specific for CC chemokine receptor-3 (CCR3) in these cells. The stimulation of these cells by eotaxin (1-100 ng/ml) dose-dependently increased eotaxin production. In addition, RANTES or eotaxin-2 but not MCP-3 at the higher concentrations (100 ng/ml), also induced slight eotaxin production. Eotaxin elicited the expression of eotaxin mRNA at 6 h after stimulation. Antibody against eotaxin or CCR3, and actinomycin D inhibited these effects of eotaxin. These antibodies also significantly inhibited the ability of eotaxin to produce further eotaxin. These findings strongly suggest that eotaxin which originates from inflammatory cells or cells resident in the airway of bronchial asthmatics can induce further production of eotaxin and participate in expansion of allergic inflammation.
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Normal human bronchial epithelial cells (NHBECs) spontaneously synthesize and store chemokines including eotaxin, RANTES, or MCP-3. We also observed the constitutive expression of mRNA specific for CC chemokine receptor-3 (CCR3) in these cells. The stimulation of these cells by eotaxin (1-100 ng/ml) dose-dependently increased eotaxin production. In addition, RANTES or eotaxin-2 but not MCP-3 at the higher concentrations (100 ng/ml), also induced slight eotaxin production. Eotaxin elicited the expression of eotaxin mRNA at 6 h after stimulation. Antibody against eotaxin or CCR3, and actinomycin D inhibited these effects of eotaxin. These antibodies also significantly inhibited the ability of eotaxin to produce further eotaxin. These findings strongly suggest that eotaxin which originates from inflammatory cells or cells resident in the airway of bronchial asthmatics can induce further production of eotaxin and participate in expansion of allergic inflammation.
Key concepts: Eotaxin, Chemokine, CCR3, Immunology, Stimulation, Inflammation, Chemistry, Biology