Neutrophil Priming State Predicts Capillary Leak after Gut Ischemia in Rats

Prevention of Leukocyte Activation by the Neutrophil Elastase Inhibitor, Sivelestat, in the Hepatic Microcirculation After Ischemia-Reperfusion

“…Administration of NEI before induction of ischemia protects against hypoxia-induced neutrophil activation; this so-called ''neutrophil priming'' has been considered to be an indispensable step in reperfusion injury [16,26,27]. However, leukocyte dynamics in the microcirculation of organs after sivelestat treatment remained unclear.…”

TLR4 Mediates Lung Injury and Inflammation in Intestinal Ischemia-Reperfusion

“…Secondary lung inflammatory response plays a key role in the pathogenesis of acute lung injury in gut I/R [13][14][15], but the mechanisms of this process are poorly understood. Accumulation of neutrophils in the lung is a prominent feature of ALI after intestinal I/R [16]. There is abundant evidence indicating that TNF-a represents a pivotal mediator in intestinal I/Rinduced lung inflammation [5,17].…”

The TLR7/8 Agonist CL097 Primes N-Formyl-Methionyl-Leucyl-Phenylalanine–Stimulated NADPH Oxidase Activation in Human Neutrophils: Critical Role of p47phox Phosphorylation and the Proline Isomerase Pin1

“…Proinflammatory agents such as cytokines (GM-CSF, TNF-a, and IL-8) alone induce a very weak oxidative response by neutrophils but strongly enhance ROS release upon exposure to a secondary stimulus such as fMLF (18). This priming effect at the infection site could facilitate the rapid elimination of the pathogen; however, excessive and uncontrolled priming could participate to the inflammatory reaction and thus be self-destructive (22,23). The priming effect has been shown to be controlled by the partial phosphorylation of p47phox (24)(25)(26), the activation of the proline isomerase 1 (Pin1) (27), and the translocation of the flavocytochrome b588 to the plasma membranes (28,29).…”