Premium
Cyclic stretch upregulates interleukin‐8 and transforming growth factor‐ β 1 production through a protein kinase C‐dependent pathway in alveolar epithelial cells
Author(s) -
YAMAMOTO HIROYUKI,
TERAMOTO HIDEMI,
UETANI KOHSAKU,
IGAWA KATSUTOSHI,
SHIMIZU EIJI
Publication year - 2002
Publication title -
respirology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 85
eISSN - 1440-1843
pISSN - 1323-7799
DOI - 10.1046/j.1440-1843.2002.00377.x
Subject(s) - transforming growth factor , tumor necrosis factor alpha , growth factor , a549 cell , medicine , interleukin , microbiology and biotechnology , stimulation , alveolar macrophage , cytokine , inflammation , lung , cancer research , macrophage , immunology , chemistry , biology , receptor , biochemistry , in vitro
Objective: Positive‐pressure mechanical ventilation can injure the lung, causing oedema and alveolar inflammation, which is termed ‘ventilator‐induced lung injury’ (VILI). We postulated that cyclic stretch upregulates the release of cytokines, which may cause lung damage, and explored which cytokines were released after cyclic stretch in type II alveolar epithelial cells (A549). Methodology: To test this hypothesis, A549 cells were cultured on a silicoelastic membrane and interleukin (IL)‐1β, IL‐8, granulocyte–macrophage colony stimulating factor, activin, transforming growth factor (TGF)‐β1, insulin‐like growth factor‐2 and tumour necrosis factor‐α mRNA and protein were assessed after stimulation of the cells by cyclic stretch. Results: Cyclic stretch induced activation of protein kinase C and resulted in the release of IL‐8 and TGF‐β1 from A549 cells. Conclusions: The release of IL‐8 and TGF‐β1 from alveolar epithelial cells may be a contributing factor in alveolitis associated with VILI.