pci-32765 and Endotoxemia

TLR4 signaling via endotoxemia in macrophages promotes macrophage transition to the inflammatory phenotype through NLRP3 inflammasome activation. This transition event has the potential to trigger acute lung injury (ALI). However, relatively little is known about the regulation of NLRP3 and its role in the pathogenesis of ALI. Here we interrogated the signaling pathway activated by CD38, an ectoenzyme expressed in macrophages, in preventing ALI through suppressing NLRP3 activation. Wild-type and

Topics: Acute Lung Injury; Adenine; ADP-ribosyl Cyclase 1; Agammaglobulinaemia Tyrosine Kinase; Animals; Endotoxemia; Female; Inflammasomes; Macrophages; Male; Membrane Glycoproteins; Mice; Mice, Inbred C57BL; Mice, Knockout; NF-kappa B; Piperidines; Signal Transduction