Anti-intercellular adhesion molecule-1 antibody and intercellular adhesion molecule-1 gene deficiency do not prevent pulmonary neutrophil recruitment in polymicrobial sepsis
Anti-intercellular adhesion molecule-1 antibody and intercellular adhesion molecule-1 gene deficiency do not prevent pulmonary neutrophil recruitment in polymicrobial sepsis
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DOI：
10.1097/00024382-199804000-00011
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发表时间：
1998-04-01
期刊：
影响因子：
3.1
通讯作者：
Chang, LY
中科院分区：
文献类型：
--
作者：
Que, LG;Kang, BH;Chang, LY
细胞间粘附分子（ICAM）-1在正常肺组织中组成性表达，在肺部炎症中表达增加。肺中ICAM-1表达的增加是否有助于脓毒症肺部炎症过程中中性粒细胞的隔离尚不清楚。我们在盲肠结扎穿孔（CLP）引起全身性脓毒症的小鼠中验证了这一假设。ICAM-1在CLP小鼠肺组织中的表达随时间增加而增加。肺ICAM-1上调的时间过程与肺髓过氧化物酶（MPO）活性增加和光镜下中性粒细胞隔离相关。单克隆IgG 2b大鼠抗小鼠抗体，抗ICAM-1抗体（YN 1/1.7），静脉注射剂量为3，10，或30 mg/kg，但是，没有减少肺MPO水平相比，非免疫大鼠IgG。支持这些发现，肺MPO含量在ICAM-1缺陷的小鼠进行CLP显着高于类似的治疗ICAM-1充足的小鼠。我们的研究结果表明，中性粒细胞隔离在CLP后的小鼠肺是不依赖于ICAM-1。
The intercellular adhesion molecule (ICAM)-1 is expressed constitutively in normal lungs and increased in pulmonary inflammation. Whether increased ICAM-1 expression in the lung contributes to neutrophil sequestration during lung inflammation in sepsis is unclear. We tested this hypothesis in mice after systemic sepsis from cecal ligation and puncture (CLP). ICAM-1 expression in mouse CLP lung tissue was found to increase with time. The time course of lung ICAM-1 up-regulation correlated with increases in lung myeloperoxidase (MPO) activity and neutrophil sequestration by light microscopy. The monoclonal IgG2b rat anti-mouse antibody, an anti-ICAM-1 antibody (YN1/1.7), administered intravenously at doses of 3, 10, or 30 mg/kg, however, did not decrease the lung MPO levels compared with nonimmune rat IgG. In support of these findings, lung MPO content in ICAM-1-deficient mice that underwent CLP was significantly higher than similarly treated ICAM-1-sufficient mice. Our results suggest that neutrophil sequestration in the mouse lung after CLP is not dependent on ICAM-1.