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(IFN-) and Interleukin-2 (IL-2) in rat lung epithelial cell migration and apoptosis after oxidant injury
1 Department of Medecine, Groupe de Recherche en Physiopathologie Respiratoire, Centre de Recherche Clinique, CUSE Sherbrooke, Sherbrooke, Quebec, Canada; Department of Medecine, Soins Intensifs Medicaux, Universite de Sherbrooke, Sherbrooke, Quebec, Canada
2 Department of Medecine, Groupe de Recherche en Physiopathologie Respiratoire, Centre de Recherche Clinique, CUSE Sherbrooke, Sherbrooke, Quebec, Canada; Department of Medecine, Groupe de Recherche en Geriatrie et Gerontologie, Universite de Sherbrooke, Sherbrooke, Quebec, Canada
3 Department of Medecine, Groupe de Recherche en Physiopathologie Respiratoire, Centre de Recherche Clinique, CUSE Sherbrooke, Sherbrooke, Quebec, Canada
4 Department of Medecine, Groupe de Recherche en Geriatrie et Gerontologie, Universite de Sherbrooke, Sherbrooke, Quebec, Canada
* To whom correspondence should be addressed. E-mail: Olivier.Lesur{at}USherbrooke.ca.
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 to restitution processes of the lung epithelium, functionality of IL-2R on TIIP was conditional to IFN- exposure : i) IFN- priming promoted a 5-fold increase of IL-2-driven TIIP locomotion (p<0.05 vs control at 100U/ml), ii) IFN- co-incubation with IL-2 reduced Bleomycin-induced TIIP apoptosis in vitro by 25% [caspase 3 activity] and by ~ 70% [TUNEL/DAPI assay], as well as in vivo by ~ 90% [caspase 3 activity] (p<0.05 vs control). Sustained p42/44 ERKinase activity played a protective role in this process, while specific inhibition by PD-98059 (50µM) significantly reversed Bleomycin-induced TIIP apoptosis (p<0.05 vs control). From these in vitro and in vivo data, it is proposed that combination 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 following oxidant-induced ALI.
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