MORINGA TEA BLOCKS ACUTE LUNG INFLAMMATION INDUCED BY SWINE CONFINEMENT DUST THROUGH A MECHANISM INVOLVING TNF-α EXPRESSION, C-JUN N-TERMINAL KINASE ACTIVATION AND NEUTROPHIL REGULATION

Plant based products represent a promising alternat ive to conventional treatments for inflammation. Moringa oleifera Lam is a tree rich in proteins, vitamins, minerals and a variety of phytochemcals with health benefits. Among the reported health benefits are antioxidant and anti-inflammatory properties. The purpose of th is study was to investigate whether tea brewed from dried Moringa leaves would abrogate inflammation in a mouse model of acute lung inflammation induced by LPS or extracts prepared from dust collected from a swine confinement facility (DE). Mice were offered water or Moringa tea for seven days. Tea consumption was significantly greater than that of water consumptio n on days 1 and 6, but there were no significant di fferences in weight gain or food consumption. On day seven, mice from both groups were forced to inhale, via int ranasal challenge, either Phosphate Buffered Saline (PBS), Lipopolysaccharide (LPS) [10 μg mL -1 ] or DE [10%]. Compared to mice that drank water, mice that drank Moringa tea had significantly less protein (p<0.05) and cellular influx (p<0.0001) into the lung after inha lation of 10% DE. No difference in neutrophil migra tion into the lungs of water and M. tea groups after LPS or D E challenge was detected. But mice that drank tea h ad significantly (p<0.05) more neutrophils with apopto tic morphology after DE challenge. TNF-α expression 24 h after inhalation of 10% DE, was significantly highe r (p<0.05) in lungs of M. tea mouse group as compared to water group. This increase in TNF-α was accompanied by higher levels of pro and anti-i nflammatory cytokines. Finally, activation of c-Jun N-terminal Kinase (JNK) in lungs of M. tea+DE group 24 h post inhalation was decreased. Taken together these resu lts suggest that Moringa oleifera leaf tea exerts antiinflammatory properties on acute lung inflammation induced by swine confinement dust through a mechanism involving neutrophil regulation and JNK activation.