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Cardiovascular pathologies are closely associated with intravascular thrombotic episodes, which is a complex phenomenon. Thrombosis involves continual interactions between platelets, plasma proteins and endothelial cells.

The work undertaken in my lab has been focused on these interactive participants of thrombosis. Neutrophils (PMNs), the cohabitant of platelets in blood, release several factors that alter platelet response.PMNs are one of the most imperative cells in innate immunity and are often referred to as foot soldiers of innate immune response. Their importance can be revealed by the fact that they comprise of almost 60% of total leukocyte population and are the first cells recruited to the site of infection.

Migration of PMNs from blood to specific tissues following pathological insult is a key feature of the host inflammatory response, which is often localized and protective.

These cells, however, have a very short lifespan of 6-7h; during this short life span they perform very crucial functions in host defence. Upon infection, they employ several effective antimicrobial strategies against a broad range of pathogens.

These include microbial killing, phagocytosis, degranulation, and even sacrifice themselves by process known as Neutrophil extracellular traps (NETs) release referred as NETosis. Neutrophils, the suicide killers, possess efficient oxidative and non-oxidative machineries to execute the engulfed pathogens.Activated PMNs generate highest amount of reactive oxygen species in human body through NADPH-oxidase (NOX-2) and myeloperoxidase (MPO), while resting and activated cells generate nitric oxide (NO) in appreciable amounts.

NO, a signalling molecule is a key mediator in a diverse number of physiological and pathophysiological processes as well as in the immune system. Research in our lab has been focused to understand that how this gaseous molecule strongly influences various functions of neutrophils.