Excessive Reactive Oxygen Species Inhibit IL-17A γδT Cells and Innate Cellular Responses to Bacterial Lung Infection

Abstract

Aims: Excessive reactive oxygen species (ROS) are detrimental to immune cellular functions that control pathogenic microbes; however, the mechanisms are poorly understood. Our aim was to determine the immunological consequences of increased ROS levels during acute bacterial infection. Results: We used a model of Streptococcus pneumoniae (Spn) lung infection and superoxide dismutase 3-deficient (SOD3-/-) mice, as SOD3 is a major antioxidant enzyme that catalyses the dismutation of superoxide radicals. First, we observed that in vitro, macrophages from SOD3-/- mice generated excessive phagosomal ROS during acute bacterial infection. In vivo, there was a significant reduction in infiltrating ne..