Neutrophils representing major cell types of the innate immune system are the most abundant leukocytes in circulation and combat pathogens through distinctly regulated processes such as a) degranulation and oxidative burst; b) phagocytosis and c) producing extracellular traps. Neutrophils upon activation with a wide variety of pathogens expel DNA bound with histones and granular proteins to form extracellular traps (NETs). High concentrations of antimicrobial effectors within these DNA lattices serve as a platform to activate pro-inflammatory mediators, immobilize and kill the pathogens and simultaneously clear the infection. Neutrophil recruitment at inflammatory sites and failure undergoing apoptosis and impaired clearance of dead neutrophils along with NETs components results in host tissue damage and release of pro-inflammatory cytokines. This indicates the existence of checkpoints that regulate neutrophil kinetics and fate and inability to regulate these checkpoints overt in extensive host tissue damage leading to organ dysfunction and diseases. Neutrophil mediated inflammation has been described in various diseases including Type 2 Diabetes (T2D), obesity, atherosclerosis, cancer, autoimmune diseases and inter alia. Exploring systems biology approaches using cell culture, rodent and clinical models of T2D, sepsis and stroke, our team aims to understand how NETs and associated mechanisms play significant role in T2D induced recurrent infections and vascular complications.