Interleukin (IL)-4/IL-9 and exogenous IL-16 induce IL-16 production by BEAS-2B cells, a bronchial epithelial cell line.
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.
Department of Pulmonary Medicine and Clinical Immunology, Dokkyo University School of Medicine, Tochigi, 321-0293, Japan.
N
N
Yoshida
M
M
Arima
G
G
Cheng
F
F
Eda
H
H
Hirata
K
K
Honda
F
F
Fukushima
T
T
Fukuda
D001980:Bronchi / Q000378:metabolism*; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D002460:Cell Line; D002634:Chemotaxis, Leukocyte; D004804:Eosinophils / Q000276:immunology; D004847:Epithelial Cells / Q000378:metabolism; D006801:Humans; D019410:Interleukin-16 / Q000096:biosynthesis* / Q000494:pharmacology; D015847:Interleukin-4 / Q000494:pharmacology*; D016906:Interleukin-9 / Q000494:pharmacology*; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology
D019410:Interleukin-16; D016906:Interleukin-9; D014409:Tumor Necrosis Factor-alpha; D015847:Interleukin-4