VITAMIN E BOOSTS NEUTROPHIL ELASTASE ACTIVITY AND THEIR ABILITY TO KILL STREPTOCOCCUS PNEUMONIAE

Abstract

Streptococcus pneumoniae (pneumococcus) remain a leading cause of life-threatening infections such as pneumonia, bacteremia and meningitis in the elderly. Neutrophils are innate immune cells that are key determinants of disease following infection as their presence is initially required to control bacterial numbers, but their persistence in the lungs can lead to tissue destruction and bacterial spread. We previously found that vitamin E (VE) supplementation reverses the age-associated increase in susceptibility to S. pneumoniae in mice by modulating pulmonary recruitment of neutrophils. The objective of this study was to test the effect of VE on the ability of neutrophils isolated from young (22–35 years) or elderly (65–69 years) volunteers to migrate across lung epithelial cell in response to S. pneumoniae and to kill complement-opsonized bacteria in vitro. We found no distinguishable differences in neutrophil migration from young and elderly donors and that VE diminished transepithelial migration across all ages. Surprisingly, unlike previous studies showing defective killing of antibody opsonized bacteria with aging, we found that when compared to young donors, neutrophils of older donors were better at killing complement opsonized pneumococci ex vivo. This increased antibacterial response in neutrophils from elderly individuals correlated with elevated activity of the antimicrobial serine protease neutrophil elastase. Exposure of neutrophils to VE elevated enzymatic activity of neutrophil elastase in young donors and increased pneumococcal killing by these cells. These findings demonstrate that VE is an effective modulator of innate immune cell function with potential to fight bacterial pneumonia.