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Oxidant Signaling in Lung Cells

Role of IFN- and IL-2 in rat lung epithelial cell migration and apoptosis after oxidant injury

¹Groupe de Recherche en Physiopathologie Respiratoire, ²Soins Intensifs Médicaux, and ³Groupe de Recherche en Gériatrie et Gérontologie, Université de Sherbrooke, Sherbrooke, Québec, Canada J1H 5N4

Submitted 30 October 2002 ; accepted in final form 3 August 2003

In the present study, IFN- exposure to primary cultures of rat type II epithelial cells (TIIP) upregulated membrane expression of the common -chain of the IL-2 receptor (2.5- to 4-fold increase) and redistributed receptor affinity in TIIP, as assessed by Western blot, cell, and tissue histochemistry and Scatchard analysis. As for restitution processes of the lung epithelium, functionality of IL-2R on TIIP was conditional to IFN- exposure: 1) IFN- priming promoted a fivefold increase of IL-2-driven TIIP locomotion (P < 0.05 vs. control at 100 U/ml) and 2) IFN- coincubation with IL-2 reduced bleomycin-induced TIIP apoptosis in vitro by 25% (caspase-3 activity) and by 70% (TdT-mediated dUTP nick end labeling/4',6'-diamidino-2-phenylindole assay) as well as in vivo by 90% (caspase-3 activity; P < 0.05 vs. control). Sustained p42/44 extracellular signal-regulated kinase activity played a protective role in this process, whereas specific inhibition by PD-98059 (50 µM) significantly reversed bleomycin-induced TIIP apoptosis (P < 0.05 vs. control). From these in vitro and in vivo data, it is proposed that combinations of IFN- and IL-2 can drive repair activity of TIIP by stimulating migration and preventing programmed cell death, both of which are speculated to be very fast restitution events after oxidant-induced acute lung injury.

interferon-; interleukin-2 receptor

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