Sheela Nagarkoti

TL;DR: It is demonstrated for the first time that treatment of human PMNs with oxLDL or its various oxidized phopholipid component mediated NETs release, implying their role in the pathogenesis of inflammatory diseases such as SIRS.

TL;DR: A crucial role of NO/iNOS is suggested in neutrophil apoptosis via enhanced ROS generation and caspase-8 mediated activation of mitochondrial death pathway.

TL;DR: In this paper, two major types of NETosis have been described - NOX-dependent and independent -using PMA and A23187 as the inducers of NOX dependent and NOX independent NETosis respectively.

TL;DR: Enhanced nitroxidative stress may results in LPL S-glutathionylation leading to impaired chemotaxis, polarization, and bactericidal activity of human PMNs, providing a mechanistic basis for their impaired functions in diabetes mellitus.

TL;DR: Data obtained suggest that oxidative status act as an important regulator of NO generation/iNOS expression, and under enhanced oxidative stress condition, NOX2-mtROS-NFκB S-glutathionylation is a feed forward loop, which attenuate NO generation and iNOSexpression in human PMNs.