The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Hemorrhagic shock-activated neutrophils augment TLR4 signaling- induced TLR2 upregulation in alveolar macrophages: role in hemorrhage-primed lung inflammation.

Hemorrhagic shock renders patients susceptible to the development of acute lung injury in response to a second inflammatory stimulus by as yet unclear mechanisms. We investigated the role of neutrophils (PMN) in alveolar macrophage (AMphi) priming, specifically, the role in mediating Toll-like receptor (TLR)4 and TLR2 cross talk in AMphi. Using a mouse model of hemorrhagic shock followed by intratracheal administration of LPS, we explored a novel function of shock-activated PMN in the mechanism of TLR2 upregulation induced by LPS-TLR4 signaling in AMphi. We showed that antecedent hemorrhagic shock enhanced LPS- induced TLR2 upregulation in AMphi. In neutropenic mice subjected to shock, the LPS- induced TLR2 expression was significantly reduced, and the response was restored upon repletion with PMN obtained from shock-resuscitated mice but not by PMN from sham-operated mice. These findings were recapitulated in mouse AMphi cocultured with PMN. The enhanced TLR2 upregulation in AMphi augmented the expression of macrophage inflammatory protein-2, TNF-alpha, and macrophage migration inhibitory factor in the AMphi in response to sequential challenges of LPS and peptidoglycan, a prototypical TLR2 ligand, which physiologically associated with amplified AMphi-induced PMN migration into air pouch and lung alveoli. Thus TLR2 expression in AMphi, signaled by TLR4 and regulated by shock-activated PMN, is an important positive-feedback mechanism responsible for shock-primed PMN infiltration into the lung after primary PMN sequestration.[1]


  1. Hemorrhagic shock-activated neutrophils augment TLR4 signaling-induced TLR2 upregulation in alveolar macrophages: role in hemorrhage-primed lung inflammation. Fan, J., Li, Y., Vodovotz, Y., Billiar, T.R., Wilson, M.A. Am. J. Physiol. Lung Cell Mol. Physiol. (2006) [Pubmed]
WikiGenes - Universities