Enhanced pulmonary expression of CXC chemokines during hepatic ischemia/reperfusion-induced lung injury in mice.
Enhanced pulmonary expression of CXC chemokines during hepatic ischemia/reperfusion-induced lung injury in mice.
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小鼠肝缺血/再灌注引起的肺损伤期间 CXC 趋化因子的肺部表达增强。
DOI：
10.1006/jsre.1998.5490
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发表时间：
1999
期刊：
影响因子：
--
通讯作者：
Edwards,MJ
中科院分区：
文献类型：
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作者：
Yoshidome,H;Lentsch,AB;Cheadle,WG;Miller,FN;Edwards,MJ
背景肝切除和肝移植过程中的肝脏缺血/再灌注损伤可导致局部和全身器官功能障碍。库普弗细胞在缺血/再灌注的初始阶段释放的促炎介质被认为参与了嗜中性粒细胞介导的肺损伤的发展。然而，涉及肺募集中性粒细胞的确切因素尚不清楚。本研究旨在探讨CXC趋化因子巨噬细胞炎性蛋白-2（MIP-2）和KC在肝缺血/再灌注后肺中性粒细胞募集和损伤中的作用。肺组织髓过氧化物酶（MPO）含量测定肺组织中神经元蓄积。采用RT-PCR方法检测MIP-2和KC mRNA的表达。肺水肿量化湿干重ratios. Results 3小时后，肝再灌注，血清肿瘤坏死因子-α水平升高。肺组织MIP-2和KC mRNA的表达也在此时增加。MIP-2和KC mRNA的表达在再灌注后9 h仍升高，但MIP-2 mRNA的水平明显低于再灌注后3 h。再灌注后3 h内中性粒细胞的肺募集增加，但在9 h时恢复至基线水平。再灌注后3、9 h肺水肿加重。中和MIP-2或KC抗体显着降低肺水肿9 h后reperfusion.ConclusionsThese数据表明，介质释放在肝缺血/再灌注诱导MIP-2和KC在肺中的表达。此外，MIP-2和KC似乎有助于肝缺血/再灌注后肺中性粒细胞积聚和相关的肺损伤。
BackgroundHepatic ischemia/reperfusion injury during both hepatic resection and transplantation may lead to local and systemic organ dysfunction. Proinflammatory mediators released by Kupffer cells during the initial phase of ischemia/reperfusion are thought to be involved in the development of neutrophil-mediated lung injury. However, the precise factors involved in lung recruitment of neutrophils are unclear. The objective of current study was to determine whether the CXC chemokines, macrophage inflammatory protein-2 (MIP-2) and KC, contribute to pulmonary neutrophil recruitment and injury following hepatic ischemia/reperfusion.MethodsC57BL/6 mice were subjected to 90 min of partial hepatic ischemia and 3, 6, and 9 h of reperfusion. Neutrophil accumulation in lung was assessed by lung content of myeloperoxidase (MPO). MIP-2 and KC mRNA were measured using RT–PCR. Lung edema was quantified by wet to dry weight ratios.ResultsThree hours after hepatic reperfusion, serum levels of tumor necrosis factor-α were increased. Lung expression of both MIP-2 and KC mRNA was also increased at this time. Both MIP-2 and KC mRNA expression remained elevated 9 h after reperfusion, although levels of MIP-2 mRNA were significantly lower than at 3 h. Pulmonary recruitment of neutrophils was increased within 3 h after reperfusion, but returned to baseline levels by 9 h. Lung edema was increased 3 and 9 h after reperfusion. Neutralization of MIP-2 or KC with antibody significantly decreased lung edema 9 h after reperfusion.ConclusionsThese data suggest that mediators released during hepatic ischemia/reperfusion induce the expression of MIP-2 and KC in the lung. In addition, it appears that MIP-2 and KC contribute to lung neutrophil accumulation and the associated pulmonary injury following hepatic ischemia/reperfusion.
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DOI：
--
发表时间：
1993-08
期刊：
The American journal of pathology
影响因子：
--
作者：
Andreas Seekamp;Michael S. Mulligan;Gerd O. Till;C. Smith;M. Miyasaka;T. Tamatani;rd R F Todd;P. Ward
通讯作者：
Andreas Seekamp;Michael S. Mulligan;Gerd O. Till;C. Smith;M. Miyasaka;T. Tamatani;rd R F Todd;P. Ward
IgG 免疫复合物诱导的肺损伤中对 C-X-C 趋化因子（巨噬细胞炎症蛋白 2 和细胞因子诱导的中性粒细胞趋化剂）的需求。
DOI：
--
发表时间：
1997
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Shanley,TP;Schmal,H;Warner,RL;Schmid,E;Friedl,HP;Ward,PA
通讯作者：
Ward,PA
影响因子：
15.9
作者：
COLLETTI, LM;KUNKEL, SL;STRIETER, RM
通讯作者：
STRIETER, RM
影响因子：
15.9
作者：
COLLETTI, LM;REMICK, DG;CAMPBELL, DA
通讯作者：
CAMPBELL, DA
DOI：
10.3109/10715769109105223
发表时间：
1991-01-01
期刊：
FREE RADICAL RESEARCH COMMUNICATIONS
影响因子：
--
作者：
JAESCHKE, H;BAUTISTA, AP;SPITZER, JJ
通讯作者：
SPITZER, JJ