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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]

References

  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]
 
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