Effects of extracellular ATP on bovine lung endothelial and epithelial cell monolayer morphologies, apoptoses, and permeabilities.
Effects of extracellular ATP on bovine lung endothelial and epithelial cell monolayer morphologies, apoptoses, and permeabilities.
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细胞外 ATP 对牛肺内皮和上皮细胞单层形态、凋亡和通透性的影响。
DOI：
10.1128/cvi.00282-08
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发表时间：
2009
期刊：
影响因子：
--
通讯作者：
Czuprynski,Charles
中科院分区：
文献类型：
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作者：
McClenahan,David;Hillenbrand,Kati;Kapur,Arvinder;Carlton,David;Czuprynski,Charles
牛肺炎是一种重要的疾病，无论是在经济上还是在动物福利方面。最近在其他物种中的证据表明，ATP是肺部炎症的重要调节剂，它由激活的肺泡巨噬细胞和受损的肺细胞释放。ATP在牛肺感染过程中是否也起着类似的作用尚不清楚。在本研究中，我们研究了ATP处理对牛肺上皮细胞（BPE）和牛肺微血管内皮细胞（BPMEC）的形态，凋亡和通透性的影响。当暴露于ATP时，BPE细胞的单层经历了显著的形态学变化，包括细胞的分离。无论是BPE细胞，也没有BPMEC表现出增加细胞凋亡的ATP反应。当暴露于ATP时，BPE细胞和BPMEC单层显示几乎相同的渗透性增加，在暴露的第一个小时内发生50%的变化。两种细胞类型都含有P2X7受体的mRNA，P2X7受体是一种已知的ATP受体。在BPE细胞中，而不是BPMEC中，通过加入P2X7受体拮抗剂，ATP引起的通透性变化被逆转。如果在体内发生类似的渗透性变化，则它们可能是肺炎期间血管渗漏到肺气隙中的一个因素。
Pneumonia in cattle is an important disease both economically and in terms of animal welfare. Recent evidence in other species has shown ATP to be an important modulator of inflammation in the lung, where it is released by activated alveolar macrophages and damaged lung cells. Whether ATP serves a similar process during infection in the bovine lung is unknown. In the present study, we examined the effects of ATP treatment on the morphology, apoptosis, and permeability of bovine pulmonary epithelial (BPE) cells and bovine pulmonary microvascular endothelial cells (BPMEC). Monolayers of BPE cells underwent striking morphological changes when exposed to ATP that included separation of the cells. Neither BPE cells nor BPMEC exhibited increased apoptosis in response to ATP. BPE cell and BPMEC monolayers displayed virtually identical increases in permeability when exposed to ATP, with a 50% change occurring within the first hour of exposure. Both cell types contained mRNA for the P2X7receptor, a known receptor for ATP. In BPE cells, but not BPMEC, the change in permeability in response to ATP was reversed by the addition of a P2X7receptor antagonist. If similar permeability changes occur in vivo, they could be a factor in vascular leakage into lung airspaces during pneumonia.