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N ‐acetyl‐ L ‐cysteine inhibits bleomycin‐induced interleukin‐8 secretion by bronchial epithelial cells
Author(s) -
Gon Yasuhiro,
Hashimoto Shu,
Nakayama Tomoko,
Matsumoto Ken,
Koura Toshiya,
Takeshita Ikuko,
Horie Takashi
Publication year - 2000
Publication title -
respirology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 85
eISSN - 1440-1843
pISSN - 1323-7799
DOI - 10.1111/j.1440-1843.2000.00268.x
Subject(s) - pyrrolidine dithiocarbamate , pathogenesis , bleomycin , medicine , secretion , interleukin , microbiology and biotechnology , cytokine , cancer research , immunology , inflammation , biology , nf κb , chemotherapy
Objective: Bleomycin (BLM) has proven effective for the treatment of cancers, but the most serious dose‐limiting side‐effect is the development of pulmonary toxicity. Although the precise mechanism in the pathogenesis of BLM‐induced lung injury has not been determined, oxygen radicals and neutrophils are indicated to play a key role in it. Interleukin‐8 (IL‐8) is thought to be an important mediator of the pathogenesis of acute lung injury. Methodology: The IL‐8 production from bronchial epithelial cell line, BEAS‐2B cells was measured by enzyme‐linked immunosorbent assays for IL‐8. Results: The concentrations of IL‐8 were reportedly elevated in BLM‐induced lung injury, suggesting the involvement of IL‐8 in the pathogenesis of BLM‐induced lung injury. In the present study, we showed that BLM induced the expression of IL‐8 protein and mRNA in BEAS‐2B cells, and N ‐acetyl‐ L ‐cysteine (NAC) inhibited IL‐8 expression. In addition, the structurally unrelated anti‐oxidant, pyrrolidine dithiocarbamate (PDTC) also effectively inhibited BLM‐induced IL‐8 production. Conclusion: These results suggest that anti‐oxidant‐sensitive mechanism might be involved in the inhibition of IL‐8 secretion by BLM‐stimulated bronchial epithelial cells and that NAC might be useful for the treatment of BLM‐induced lung injury.