A Bittersweet Response to Infection in Diabetes; Targeting Neutrophils to Modify Inflammation and Improve Host Immunity

Chronic and recurrent infections occur commonly in both type 1 2 diabetes (T1D, T2D) increase patient morbidity mortality. Neutrophils are professional phagocytes of the innate immune system that critical pathogen handling. Neutrophil responses to infection dysregulated diabetes, predominantly mediated by persistent hyperglycaemia; chief biochemical abnormality T1D T2D. Therapeutically enhancing host immunity improve resolution is an expanding area research. Individuals with also at increased risk severe coronavirus disease 2019 (COVID-19), highlighting need for re-invigorated urgent focus on this field. The aim review explore breadth previous literature investigating neutrophil function T2D, order understand complex phenotype present development new therapies aberrant diabetes. Existing illustrates a dual dysfunction Key handling mechanisms recruitment, chemotaxis, phagocytosis intracellular reactive oxygen species (ROS) production decreased weakening response infection. However, pro-inflammatory pathways, mainly extracellular trap (NET) formation, ROS generation cytokine generation, significantly upregulated, causing damage perpetuating inflammation. Reducing these proinflammatory outputs therapeutically emerging as credible strategy more recently COVID-19. Future research needs drive forward exploration novel treatments T2D