2000International Archives of Allergy and ImmunologyRequires access

Autocrine Regulation of Eotaxin in Normal Human Bronchial Epithelial Cells

Hiroshi Saito, Hisako Shimizu, Kazuo Akiyama

Open publisher page 10 citations

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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What this paper is about

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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Available 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.

Key concepts: Eotaxin, Chemokine, CCR3, Immunology, Stimulation, Inflammation, Chemistry, Biology

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