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Severe bacterial infection or trauma frequently leads to a systemic inflammatory response, a self-reinforcing activation of neutrophils and vascular endothelial cells that can be deadly. On page 641, Cepinskas et al. describe a neutrophil-mediated signaling mechanism that inhibits inflammation. The findings demonstrate a novel function for neutrophils and a previously unknown form of immunological tolerance, and they identify a promising target for new anti-inflammatory drugs." r3 z$ d7 a1 ~# Z9 r
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In systemic inflammation, circulating cytokines cause the transcription factor NFB to translocate from the cytoplasm to the nucleus of vascular endothelial cells, where it induces the transcription of pro-inflammatory genes. Using a cell culture model of inflammation, the authors found that the migration of neutrophils across a monolayer of cytokine-activated endothelial cells causes NFB levels in the endothelial cell nuclei to drop. Cross-linking the adhesion molecule PECAM-1 on the surface of the endothelial cells produces the same effect, suggesting that the neutrophils send anti-inflammatory signals to the endothelium through PECAM-1. Exposing the neutrophil-calmed endothelial cells to a second round of cytokine activation results in even further reduction of the pro-inflammatory response. The authors are now trying to determine what controls this novel type of induced tolerance at the molecular level.(Transendothelial migration of neutrophil) |
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发表于 2009-3-6 00:43
发表于 2015-6-5 19:35
