Inhibition of mammalian target of rapamycin aggravates the respiratory burst defect of neutrophils from decompensated patients with cirrhosis
Loïc Rolas, Nesrine Makhezer, Soumeya Hadjoudj, Jamel El‐Benna, Bahia Djerdjouri, Laure Elkrief, Richard Moreau, Axel Périanin – 18 October 2012 – Cirrhosis is commonly accompanied by impaired defense functions of polymorphonuclear leucocytes (PMNs), increased patient susceptibility to infections, and hepatocellular carcinoma (HCC). PMN antimicrobial activity is dependent on a massive production of reactive oxygen species (ROS) by nicotinamide adenine dinucleotide phosphate (NADPH) 2 (NADPH oxidase 2; NOX2), termed respiratory burst (RB).