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Role of nNOS in the progression of systemic inflammatory response induced by lipopolysaccharide

Nitric oxide synthases (nNOS, eNOS & iNOS) are a family of enzymes that catalyze the production of nitric oxide (NO) from L‐arginine. NO is an important cellular signaling molecule, having a vital role in many biological processes. The roles of eNOS (endothelial NOS) and iNOS (inducible NOS) in mediating inflammatory processes have been appreciated but little is available about the role of nNOS (neuronal NOS) especially in what pertains to the initiation of the inflammatory process. Our recent findings suggest that nNOS‐KO mice are resistant to LPS induced inflammation. To gauge the molecular mechanism we have identified that inhibition of nNOS leads to over expression of SOCS1 and elevated SOCS1 binding to P65 subunit of NFkB within the nucleus. SOCS1 operating as a ubiquitin ligase, targets nuclear p65 to degradation. In addition, serine phosphorylation at various sites of the p65 subunit has been shown to be important in initiating transcription. We have also shown that decreased phosphorylation of p65(536) in nNOS‐ko cells after LPS stimulation results in transcriptional inactivation of p65 subunit of NfkB. Thus these molecular events provide terminated expression of NfkB inducible genes and LPS tolerance in nNOS‐ko mice. Taking together our recent studies pointing towards the important role played by nNOS in the initiation of inflammatory response and ultimately in lung injury, sepsis and mortality.