Type 2 Diabetes is major risk factor for upper respiratory tract infections. Impairments in innate immune cells have been shown to contribute significantly to the observed susceptibility. In particular, diabetes, is associated with several impairments in neutrophil functions, including migration, ROS production, phagocytosis, and bacterial killing, which all together contribute to high incidence of bacterial infections. Neutrophils kill pathogen both intracellularly via Phagocytosis and extracellularly via NETosis. However, conditions/factors that allow for the selection of phagocytosis or NETosis remains elusive. While there is evidence that both phagocytosis and NETosis might be occurring simultaneously, the exact mechanism governing the two still remains unclear. Neutrophils are known to produce microvesicles and exosomes during phagocytosis, which are small intact vesicles of different sizes. They can contain membrane, cytoplasmic and nuclear components of the parent cell and typically retain surface markers of their parent cells. The micro-vesicles bind to resting neutrophils via TLR4; however, the downstream effect of this interaction remains to be elucidated. In previous, activation and engagement of TRL4 have been shown to induce ROS generation, which is central to induction of Neturophil extracellular traps (NETs). To understand the effect of this binding we propose to test the following hypothesis; “Hyperglycemia induced microvesicles and exosomes in neutrophils can bind to neighboring neutrophils via TLR4 and stimulate NETosis”. To test this hypothesis, we developed the following aims (i) to investigate microvesicles and exosomes formation by neutrophils in hyperglycemic and normal glycemic conditions, (ii) To determine if hyperglycemia induced microvesicles and exosomes from neutrophils induce NETs in resting neutrophils. Our results confirmed the induction of NETosis in the presence of hyperglycemia induced microvesicles and exosomes. Moreover, high level of exosomes was observed in hyperglycemic conditions as compared to normal.