Pulmonary and extrapulmonary acute lung injury: inflammatory and ultrastructural analyses

Pulmonary and extrapulmonary acute lung injury: inflammatory and ultrastructural analyses
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DOI:
10.1152/japplphysiol.01182.2004
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发表时间:
2005-05-01
影响因子:
3.3
通讯作者:
Rocco, PRM
Rocco, PRM
中科院分区:
医学2区
文献类型:
--
作者:
Menezes, SLS;Bozza, PT;Rocco, PRM

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目的:探讨肺内和肺外急性肺损伤(ALI)在相同机械损伤时是否表现出不同的形态学改变和免疫学通路。为此,建立了具有相似功能变化的肺(p)和肺外(ex)ALI模型,并分析了肺形态(光镜和电镜)、细胞因子水平、支气管肺泡灌洗液(BALF)中的中性粒细胞浸润、弹性和胶原纤维含量。肺泡隔,以及肺实质中的中性粒细胞凋亡。BALB/c小鼠分为4组。对照组分别腹腔注射生理盐水(0.5ml)和气管内滴注生理盐水(0.05ml)。在ALIp和ALIexp组中,小鼠接受E.大肠杆菌脂多糖(分别为10 μ g it和125 μ g ip)。在ALIp和ALIexp组中,肺阻力和粘弹性压力以及静态弹性、肺泡塌陷和肺组织中细胞含量的变化相似。与ALIexp相比,ALIp组BALF中KC(IL-8的鼠功能同源物)和IL-10水平增加了3倍,而IL-6水平显示ALIp增加了2倍。BALF中的中性粒细胞在ALIp中比在ALIexp中更常见。ALIp组肺泡上皮、完整的毛细血管内皮和凋亡的中性粒细胞的损伤更广泛,而ALIexp组则表现为间质性水肿和完整的I型和II型细胞和内皮层。总之,由于相同的肺机械功能障碍的病因独立的ALI,在肺上皮损伤产生了更明显的炎症反应,诱导超微结构形态学的变化。
To test whether pulmonary and extrapulmonary acute lung injury (ALI) of identical mechanical compromise would express diverse morphological patterns and immunological pathways. For this purpose, a model of pulmonary ( p) and extrapulmonary (exp) ALI with similar functional changes was developed and pulmonary morphology ( light and electron microscopy), cytokines levels, and neutrophilic infiltration in the bronchoalveolar lavage fluid (BALF), elastic and collagen fiber content in the alveolar septa, and neutrophil apoptosis in the lung parenchyma were analyzed. BALB/c mice were divided into four groups. In control groups, saline was intratracheally ( it, 0.05 ml) instilled and intraperitoneally (ip, 0.5 ml) injected, respectively. In the ALIp and ALIexp groups, mice received E. coli lipopolysaccharide ( 10 mu g it and 125 mu g ip, respectively). The changes in lung resistive and viscoelastic pressures and in static elastance, alveolar collapse, and cell content in lung tissue were similar in the ALIp and ALIexp groups. The ALIp group presented a threefold increase in KC ( murine function homolog to IL-8) and IL-10 levels in the BALF in relation to ALIexp, whereas IL-6 level showed a twofold increase in ALIp. Neutrophils in the BALF were more frequent in ALIp than in ALIexp. ALIp showed more extensive injury of alveolar epithelium, intact capillary endothelium, and apoptotic neutrophils, whereas the ALIexp group presented interstitial edema and intact type I and II cells and endothelial layer. In conclusion, given the same pulmonary mechanical dysfunction independently of the etiology of ALI, insult in pulmonary epithelium yielded more pronounced inflammatory responses, which induce ultrastructural morphological changes.