Jean Parodo

TL;DR: In this paper, the authors examined the hypothesis that an injurious ventilatory strategy may lead to end-organ epithelial cell apoptosis and organ dysfunction, and showed that a lung protection strategy led to increased rates of epithelialcell apoptosis in the kidney.

TL;DR: PBEF is identified as a novel inflammatory cytokine that plays a requisite role in the delayed neutrophil apoptosis of clinical and experimental sepsis and is also upregulated in neutrophils by IL-1beta and functions as an inhibitor of apoptosis in response to a variety of inflammatory stimuli.

TL;DR: Circulating neutrophils from patients with SIRS or from patients who have undergone major elective surgery show delayed expression of constitutive programmed cell death, and antiapoptotic factors are present in the general circulation.

TL;DR: Apoptosis of circulating neutrophils from patients with clinical sepsis is profoundly suppressed, through a mechanism that involves activation of nuclear factor-κB that is associated with reduced activity of caspases-9 and -3 and maintenance of mitochondrial transmembrane potential and that differs in important respects from the inhibitory effects seen following the exposure of healthy neutrophil to inflammatory stimuli.

TL;DR: It is shown that two different proinflammatory stimuli, LPS and granulocyte-macrophage-CSF, up-regulate the expression of both ICE and IL-1β in human polymorphonuclear neutrophils, and that the ICE-dependent cleavage of pro-IL-1 β results in delayed expression of the constitutive cell death program.