OBJECTIVECigarette smoke extract (CSE) can induce injuries of pulmonary II epithelial cells, activate nuclear factor-kappaB and increase tumor necrosis factor-alpha(TNF-alpha) secretion. This study aimed to investigate whether azithromycin can protect pulmonary II epithelial cells from injuries induced by CSE and relevant mechanisms.

METHODSPulmonary II epithelial cells (A549 cells) were cultured in vitro. After 48 hrs of culture the cells were randomly treated with serum-free DMEM only (blank control group), azithromycin + serum-free DMEM, CSE+ serum-free DMEM or CSE+azithromycin. Eight hours later the morphology of A549 cells, the activity of NF-kappaB and the levels of TNF-alpha were measured by inverted microscope, immunohistochemistry and ELISA.

RESULTSThe morphology and structure of A549 cells were changed, NF-kappaB activity increased (dark brown staining ) and TNF-alpha levels (0.307 +/- 0.036 pg/mL vs 0.234 +/- 0.028 pg/mL)increased in the CSE+ serum-free DMEM group compared with the blank control group (P < 0.01). CSE together with azithromycin treatment recovered partly the morphological injuries of A549 cells. It also attenuated NF-kappaB staining and decreased TNF-alpha levels from 0.307 +/- 0.036 pg/mL (CSE+serum-free DMEM group) to 0.269 +/- 0.009 pg/mL (P < 0.05).

CONCLUSIONSAzithromycin may inhibit NF-kappaB activity, decrease TNF-alpha secretion and thus lessen cytotoxicity of CSE to A549 cells.