1. Interleukin (IL)-4/IL-9 and exogenous IL-16 induce IL-16 production by BEAS-2B cells, a bronchial epithelial cell line
- Author
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Takeshi Fukuda, Fukiko Eda, Kyoko Honda, Hirokuni Hirata, Gang Cheng, Masafumi Arima, Fumiya Fukushima, and Nozomi Yoshida
- Subjects
CD4-Positive T-Lymphocytes ,Interleukin-16 ,Tumor Necrosis Factor-alpha ,Immunology ,Interleukin-9 ,Bronchi ,Epithelial Cells ,Biology ,respiratory tract diseases ,Cell Line ,Interleukin 22 ,Eosinophils ,Interleukin 21 ,Chemotaxis, Leukocyte ,Interleukin 31 ,Interleukin 13 ,Interleukin 12 ,Humans ,Interleukin 9 ,Interleukin 8 ,Interleukin-4 ,Interleukin 3 - Abstract
Previous studies have suggested that bronchial epithelial cells may perpetuate airway inflammation. We have reported that the bronchial epithelial cell line BEAS-2B can produce interleukin (IL)-16, a potent chemoattractant for CD4+ T cells. IL-16 is thought to regulate airway inflammation in asthmatics. Recent studies showed that IL-4 induces inflammatory cytokines in bronchial epithelial cells and that IL-9 is a candidate gene for development of asthma. The present study demonstrated that BEAS-2B cells produced specifically IL-16 by synergistic effects of IL-4 + IL-16, or IL-9 + IL-16, and that the synthesized IL-16 induced migration of CD4+ T cells. This study is a first report indicating that IL-16 production may be maintained by an autocrine machinery by epithelial cell-derived IL-16 with IL-4 and IL-9 in asthma.
- Published
- 2001