Role of alveolar macrophages in the regulation of local and systemic inflammation after lung contusion
Role of alveolar macrophages in the regulation of local and systemic inflammation after lung contusion
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DOI：
10.1097/ta.0b013e3182aaa499
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发表时间：
2014-02-01
影响因子：
3.4
通讯作者：
Seitz, Daniel H.
中科院分区：
文献类型：
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作者：
Niesler, Ulrike;Palmer, Annette;Seitz, Daniel H.
背景：钝性胸部创伤是一种会增加发病率和死亡率的损伤，特别是在多发伤的情况下。我们以前的研究表明，小鼠胸部钝伤后局部和全身炎症改变。本研究的目的是确定是否肺泡巨噬细胞（AM Phi）在此创伤后inflammatory.METHODS：AM Phi的雄性C3 H/HeN小鼠被耗尽氯膦酸盐脂质体滴入肺前钝性胸部创伤由一个单一的冲击波诱导。在支气管肺泡灌洗中，肺匀浆、血浆和枯否细胞、外周血单核细胞、脾巨噬细胞和脾细胞的细胞培养上清液在胸部创伤后2小时或24小时分离，通过多重测定或酶联免疫吸附测定测定介质浓度。在支气管肺泡灌洗中，AM Phi耗竭导致单核细胞趋化蛋白1和调节性和正常T细胞表达和分泌（RANTES）增加浓度以及胸部创伤后白细胞介素6浓度的减弱增加。支气管肺泡灌洗角质形成细胞衍生的趋化因子浓度增加，但非创伤性AM Phi耗尽的动物，胸部创伤后没有进一步的变化。肺匀浆中的细胞因子浓度以与创伤后早期支气管肺泡灌洗相同的方式改变。在AM Phi耗尽动物的血浆中，白细胞介素6浓度在胸部创伤后略有下降。AM Phi的耗尽消除了创伤诱导的枯否细胞趋化因子释放的减少。血单核细胞，脾巨噬细胞，脾细胞上清液中的细胞因子浓度不受AM Phi depletion.CONCLUSION：这些消耗实验表明，AM Phi改善钝性胸部创伤后的炎症反应。综上所述，本研究提供了相关的见解AM Phi在肺挫伤后局部和全身炎症的调节作用。版权所有（C）2014由Lippincott威廉姆斯& Wilkins
BACKGROUND: Blunt chest trauma is an injury that enhances the morbidity and mortality rate, particularly in the context of polytrauma. Our previous studies showed local and systemic inflammatory alterations after blunt chest trauma in mice. This study was designed to determine whether alveolar macrophages (AM Phi) have an alleviative role in this posttraumatic inflammation.METHODS: AM Phi of male C3H/HeN mice were depleted by instillation of clodronate liposomes into the lung before blunt chest trauma induced by a single blast wave. In bronchoalveolar lavage, lung homogenates, plasma, and cell culture supernatants of Kupffer cells, peripheral blood mononuclear cells, splenic macrophages, and splenocytes isolated 2 hours or 24 hours after chest trauma mediator concentrations were determined by multiplex assay or enzyme-linked immunosorbent assay.RESULTS: In bronchoalveolar lavage, AM Phi depletion led to increased monocyte chemoattractant protein 1 and regulated and normal T cell expressed and secreted (RANTES) concentrations as well as an attenuated increase of interleukin 6 concentrations after chest trauma. Bronchoalveolar lavage keratinocyte-derived chemokine concentrations increased in nontraumatized but AM Phi-depleted animals with no further change after chest trauma. Cytokine concentrations in lung homogenates were altered in the same way as in bronchoalveolar lavage early after trauma. In the plasma of AM Phi-depleted animals, interleukin 6 concentrations were slightly decreased after chest trauma. Depletion of AM Phi abrogated the trauma-induced decrease of Kupffer cell chemokine release. Cytokine concentrations of blood monocytes, splenic macrophages, and splenocyte supernatants were not influenced by AM Phi depletion.CONCLUSION: These depletion experiments show that AM Phi ameliorate the inflammatory response after blunt chest trauma. Taken together, this study gives relevant insights into the regulative role of AM Phi during the local and systemic inflammation after lung contusion. Copyright (C) 2014 by Lippincott Williams & Wilkins