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Inflammation and ischemia-induced lung angiogenesis

机译：炎症和局部缺血诱导的肺血管生成

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First published December 21, 2007; doi:10.1152/ajplung.00369.2007.-A role for inflammation in modulating the extent of angiogenesis has been shown for a number of organs. The present study was undertaken to evaluate the importance of leukocyte subpopulations for systemic angiogenesis of the lung after left pulmonary artery ligation (LPAL) in a mouse model of chronic pulmonary thromboembolism. Since we (24) previously showed that depletion of neutrophils did not alter the angiogenic outcome, we focused on the effects of dexamethasone pretreatment (general anti-inflammatory) and gadolinium chloride treatment (macrophage inactivator) and studied Rag-l~(-/-) mice (T/B lymphocyte deficient). We measured inflammatory cells in bronchoal-veolar lavage fluid and lung homogenate macrophage inflammatory protein-2 (MIP-2) and IL-6 protein levels within 24 h after LPAL and systemic blood flow to the lung 14 days after LPAL with labeled microspheres as a measure of angiogenesis. Blood flow to the left lung was significantly reduced after dexamethasone treatment compared with untreated control LPAL mice (66% decrease; P < 0.05) and significantly increased in T/B lymphocyte-deficient mice (88% increase; P < 0.05). Adoptive transfer of splenocytes (T/B lymphocytes) significantly reversed the degree of angiogenesis observed in the Rag-l~(-/-) mice back to the level of control LPAL. Average number of lavaged macrophages for each group significantly correlated with average blood flow in the study groups (r2 = 0.9181; P = 0.01 different from 0). Despite differences in angiogenesis, left lung homogenate MTP-2 and IL-6 did not differ among study groups. We conclude that inflammatory cells modulate the degree of angiogenesis in this lung model where lymphocytes appear to limit the degree of neovascularization, whereas monocytes/macrophages likely promote angiogenesis.
机译：首次发布于2007年12月21日; doi：10.1152 / ajplung.00369.2007.-许多器官已显示出炎症在调节血管生成程度中的作用。本研究旨在评估慢性肺血栓栓塞症小鼠模型中左肺动脉结扎（LPAL）后白细胞亚群对肺部系统性血管生成的重要性。由于我们（24）先前显示嗜中性白血球的消耗不会改变血管生成的结果，因此我们集中于地塞米松预处理（一般抗炎）和氯化g治疗（巨噬细胞灭活剂）的作用，并研究了Rag-1〜（-/- ）小鼠（T / B淋巴细胞不足）。我们在LPAL后24小时内测量支气管肺泡灌洗液中的炎性细胞和肺匀浆巨噬细胞炎性蛋白2（MIP-2）和IL-6蛋白水平，并在LPAL后14天内将全身血流至肺部，并标记微球血管生成的量度。与未治疗的对照组LPAL小鼠相比，地塞米松治疗后流向左肺的血流量显着减少（减少66％; P <0.05），在T / B淋巴细胞缺乏的小鼠中显着增加（增加88％; P <0.05）。脾细胞（T / B淋巴细胞）的过继转移显着逆转了在Rag-1-（-/-）小鼠中观察到的血管生成程度，回到了对照LPAL水平。每组灌洗的巨噬细胞的平均数量与研究组的平均血流量显着相关（r2 = 0.9181; P = 0.01，与0差异）。尽管在血管生成方面存在差异，但研究组之间的左肺匀浆MTP-2和IL-6并无差异。我们得出的结论是，在这种肺部模型中，淋巴细胞似乎限制了新血管形成的程度，而炎症细胞调节了血管新生的程度，而单核细胞/巨噬细胞可能促进了血管新生。

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