Mycobacterium bovis Bacillus Calmette-Guérin (BCG) stimulates IL-10 production via the PI3K/Akt and p38 MAPK pathways in human lung epithelial cells.
作者： Patricia Méndez-Samperio , Artemisa Trejo , Aline Pérez
DOI: 10.1016/J.CELLIMM.2008.03.002
关键词:
摘要: Infection of human cells with mycobacteria has been shown to result in the production anti-inflammatory cytokines. However, signaling pathways that regulate Mycobacterium bovis BCG-induced interleukin (IL)-10 are currently unknown. In present study, we investigated involvement phosphatidylinoditol 3-kinase (PI3K)/Akt and p38 MAPK secretion IL-10 lung epithelial (A549) after infection M. BCG. Treatment A549 LY 294002 (2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one) wortmannin, two PI3K inhibitors, inhibited production. Stimulation BCG caused an increase Akt phosphorylation a time-dependent manner, which was by wortmannin. addition, treatment inhibitor significantly blocked Moreover, SB203580 decreased dose-dependent whereas completely unaffected MEK PD98059. Finally, inhibition did not affect activation BCG-infected cells, indicating activity is required for MAPK. Collectively, these data suggest PI3K/Akt play important role regulation cells.
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