Meconium Aspiration Syndrome (MAS) continues to be associated with a high mortality rate and significant pulmonary morbidity. The pathophysotogy of MAS is related to the physical and chemical components of meconium which result in chemical pneumonitis and impaired surfactant function. The mechanism by which meconium induces this lung injury is not well understood. We hypothesized that this injury is mediated in part by proinflammatory cytokines produced by the alveolar macrophages (AM) in response to the meconium. AM were harvested from the lungs of 4 sets of adult C3H/HEN mice. They were pooled and placed in media containing 10% fetal calf serum at a concentration of 105 cells per well. The study cells were incubated with solutions of either 2% or 10% sterile human meconium. The control cells were incubated with either Lipopolysaccharide (LPS) or media. Supematants obtained at 4 hours were assayed for IL-6 and supematants obtained at 24 hours were assayed for IL-6 and PGE2 using commercial ELISA kits. Data were analyzed using an unpaired t test and expressed as mean ± SEM. Time Media Control LPS Control 2% Meconium 10% Meconium IL-6 pg/ml 4 hrs 27 ± 19 147 ± 41* 29 ± 13 28 ± 5 IL-6 pg/ml 24 hr. 4.2 ± 2.3 917 ± 252* 13 ± 3.5* 40 ± 4* PGE2 pg/ml 24 hrs 113 ± 52 189 ± 80 485 ± 66* 1525 ± 109** * = p <0.05 vs media control ** = p <0.001 vs media control. These findings demonstrate that meconium stimulates a dose dependent production of IL-6 by AM at 24 hours. In addition, there is also a significant dose dependent increase in PGE2 production by AM at 24 hours. Alveolar macrophage cytokine production may play a significant role in meconium induced lung injury.
|Original language||English (US)|
|Journal||Journal of Investigative Medicine|
|State||Published - 1996|
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)