Persistent neutrophil dysfunction and suppression of acute lung injury in mice following cecal ligation and puncture sepsis.
Persistent neutrophil dysfunction and suppression of acute lung injury in mice following cecal ligation and puncture sepsis.
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DOI：
10.1159/000362554
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发表时间：
2014
影响因子：
5.3
通讯作者：
Ward PA
中科院分区：
文献类型：
--
作者：
Grailer JJ;Kalbitz M;Zetoune FS;Ward PA
人和啮齿类动物的脓毒症与持续的免疫抑制有关，并伴有脓毒症急性期先天免疫缺陷。通过盲肠结扎和穿孔（CLP），随后诱导急性肺损伤，采用IgG免疫复合物的远端气道沉积，使小鼠脓毒症，以定量评估诱导脓毒症后的先天免疫应答。先天性免疫反应的抑制发生在肺早在CLP后12小时和长达21天之后。先天性免疫缺陷的机制包括减少白蛋白漏入肺部，以及支气管肺泡灌洗液中肿瘤坏死因子水平降低和持续的白细胞介素-10水平升高。CLP小鼠骨髓来源的中性粒细胞（PMN）的活化标志物CD 11b水平也降低，体外刺激后呼吸爆发抑制。这些结果在患有内毒素血症的小鼠中没有观察到，其中先天性炎症反应被保留。然而，持续的淋巴细胞减少症存在于两种模型中，这表明在两种脓毒症模型中先天性和适应性免疫的差异调节。这些数据表明，CLP诱导长期抑制炎症反应，在肺和全身，定义为骨髓来源的PMN功能障碍。
Sepsis both in humans and rodents is associated with persistent immunosuppression, accompanied by defects in innate immunity during the acute phase of sepsis. Mice were rendered septic by cecal ligation and puncture (CLP) followed by induction of acute lung injury, employing distal airway deposition of IgG immune complexes, in order to quantitatively evaluate innate immune responses following induction of sepsis. Suppression of innate immune responses in lung occurred as early as 12 hours after CLP and up to 21 days thereafter. The mechanism of innate immune defects included reduced leak of albumin into lungs together with reduced levels of tumor necrosis factor in bronchoalveolar lavage fluids and increased levels of interleukin-10 that were persistent. Bone marrow-derived neutrophils (PMNs) from CLP mice also had reduced levels of the activation marker CD11b, and a depressed respiratory burst following stimulation in vitro. These results were not observed in mice with endotoxemia, where the innate inflammatory response was preserved. However, sustained lymphopenia was present in both models, suggesting differential regulation of innate and adaptive immunity in the two sepsis models. These data indicate that CLP induced a prolonged suppression of inflammatory responses both in lung and systemically, as defined by bone marrow-derived PMN dysfunction.
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影响因子：
32.4
作者：
Riedemann, NC;Guo, RF;Ward, PA
通讯作者：
Ward, PA
严重钝性创伤后，持续的炎症，免疫抑制和分解代谢综合征。
DOI：
10.1097/ta.0b013e3182ab1ab5
发表时间：
2014-01
期刊：
The journal of trauma and acute care surgery
影响因子：
--
作者：
Vanzant EL;Lopez CM;Ozrazgat-Baslanti T;Ungaro R;Davis R;Cuenca AG;Gentile LF;Nacionales DC;Cuenca AL;Bihorac A;Leeuwenburgh C;Lanz J;Baker HV;McKinley B;Moldawer LL;Moore FA;Efron PA
通讯作者：
Efron PA
影响因子：
3.7
作者：
Liao Y;Liu P;Guo F;Zhang ZY;Zhang Z
通讯作者：
Zhang Z
影响因子：
4.8
作者：
Huber-Lang, MS;Riedeman, NC;Ward, PA
通讯作者：
Ward, PA
影响因子：
8.8
作者：
Angus, D C;Linde-Zwirble, W T;Pinsky, M R
通讯作者：
Pinsky, M R