作者: Olivier Dauwalder , Alexandre Pachot , Marie Angélique Cazalis , Malick Paye , Caroline Faudot
DOI: 10.1016/J.MICPATH.2009.07.001
关键词:
摘要: The severity of Staphylococcus aureus sepsis is positively associated with staphylococcal enterotoxin A (SEA) and negatively the gene cluster (egc), which encodes five enterotoxins (SE). It was recently demonstrated that SE can induce human leukocytes to release inflammatory mediators. Contrary SEG (one egc superantigens), SEA induces a strong proinflammatory/Th1 response, including tumor necrosis factor-alpha macrophage protein-1 alpha production. Here, we investigated very early transcriptional response PBMC these two SEs. We confirm more potent than SEG. Importantly, our data also suggest likely induced by T cells monocytes. In addition, negative feedback control triggered at same time as proinflammatory processes (inflammation apoptosis). confirms molecular level new models pathophysiology concomitant opposite sides given mechanism participating bacterial compound are both necessary. This preliminary study highlights potential studies for unraveling mechanisms leukocyte responses SE. Further needed understand underlying putative synergy between other components.