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augments in vitro alveolar epithelial
repair
Cardiovascular Research Institute, University of California, San Francisco, California 94143-0130
Biologically active interleukin (IL)-1
is present in the pulmonary
edema fluid obtained from patients with acute lung injury and has been
implicated as an important early mediator of nonpulmonary epithelial
wound repair. Therefore, we tested the hypothesis that IL-1 would
enhance wound repair in cultured monolayers from rat alveolar
epithelial type II cells. IL-1 (20 ng/ml) increased the rate of in
vitro alveolar epithelial repair by 118 ± 11% compared with that
in serum-free medium control cells (P < 0.01). IL-1 induced cell spreading and migration at the edge of the wound but not
proliferation. Neutralizing antibodies to epidermal growth factor (EGF)
and transforming growth factor-
or inhibition of the EGF receptor by
tyrphostin AG-1478 or genistein inhibited IL-1-induced alveolar
epithelial repair, indicating that IL-1 enhances in vitro alveolar
epithelial repair by an EGF- or transforming growth
factor--dependent mechanism. Moreover, the mitogen-activated protein
kinase pathway is involved in IL-1-induced alveolar epithelial repair because inhibition of extracellular signal-regulated kinase activation by PD-98059 inhibited IL-1-induced alveolar epithelial repair. In conclusion, IL-1 augments in vitro alveolar epithelial repair, indicating a possible novel role for IL-1 in the early repair process of the alveolar epithelium in acute lung injury.
alveolar type II epithelial cells; wound repair; epidermal growth
factor; transforming growth factor-
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