Hemorrhagic shock augments lung endothelial cell activation: role of temporal alterations of TLR4 and TLR2

• DOI: 10.1152/ajpregu.00445.2009
• Publication Date: 2009-10-15T02:15:27Z
• Authors: Yuehua Li; Meng Xiang; Youzhong Yuan; Guozhi Xiao; Jian Zhang; Yong Jiang; Yoram Vodovotz; Timothy R. Billiar; Mark A. Wilson; Jie Fan
• Keywords: HMGB1

Hemorrhagic shock (HS) due to major trauma predisposes the host development of acute lung inflammation and injury. The vascular endothelium is an active organ that plays a central role in injury through generating reactive oxygen species synthesizing releasing number inflammatory mediators, including leukocyte adhesion molecules regulate neutrophils emigration. Previous study from our laboratory has demonstrated setting sepsis, toll-like receptor-4 (TLR4) signaling can induce TLR2 expression endothelial cells (ECs), thereby increasing cells' response ligands. present tested hypothesis TLR4 activation by HS resultant increased surface ECs might contribute mechanism underlying HS-augmented ECs. results show high-mobility group box 1 (HMGB1) mediates HS-induced mouse (MLVECs). Furthermore, demonstrate HMGB1 induces NAD(P)H oxidase ICAM-1 lung, MLVECs sequentially depend on early phase late following HS. Finally, data indicate important enhancing augmenting pulmonary neutrophil infiltration agonist peptidoglycan. Thus, induction ECs, induced mediated HMGB1/TLR4 signaling, responsible for cell-mediated hemorrhage.