Mycoplasma pulmonis inhibits electrogenic ion transport across murine tracheal epithelial cell monolayers.
Mycoplasma pulmonis inhibits electrogenic ion transport across murine tracheal epithelial cell monolayers.
复制标题
肺支原体抑制跨小鼠气管上皮细胞单层的生电离子传输。
DOI：
10.1128/iai.66.1.272-279.1998
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发表时间：
1998
影响因子：
3.1
通讯作者：
Bridges,RJ
中科院分区：
文献类型：
--
作者：
Lambert,LC;Trummell,HQ;Singh,A;Cassell,GH;Bridges,RJ
小鼠慢性呼吸系统疾病的特征是肺支原体持续定植于气管和支气管上皮细胞表面，粘膜下和腔内免疫和炎症细胞，以及呼吸道活动改变。以确定FM的直接作用。在没有免疫和炎症细胞反应的情况下，原代小鼠气管上皮细胞单层(MTE)被顶端感染，并在Ussing小室中进行检测。感染肺支原体的MTE，而不是那些感染非鼠支原体的MTE，显示出对阿米洛利敏感的Na+吸收、环磷酸腺苷和胆碱能刺激的Cl-−分泌和跨上皮阻力的减少。这些影响被证明需要活的生物体与单层的顶面相互作用，并且依赖于生物体的数量和感染的持续时间。由于汤姆的缘故改变了交通方式。肺气肿不仅仅是上皮细胞死亡的结果，如下所示：(I)Na+和Cl-−的主动运输，尽管速率降低；(Ii)正常的细胞形态，包括完整的紧密连接，如电子显微镜所示；(Iii)平均跨上皮阻力维持在440Ω/cm~2；以及(Iv)没有液体从单层的基底外侧渗漏到顶面。在体外，上皮离子转运的改变与肺清除受损和气道功能改变是一致的。感染肺吸虫的动物。此外，还提高了学生的自学能力。肺吸虫在不杀死宿主细胞的情况下改变运输可能解释了它成功地寄生在宿主中并长期存在的原因。进一步研究了MTE-M。肺脏模型应阐明介导跨上皮离子转运减少的分子机制。
Murine chronic respiratory disease is characterized by persistent colonization of tracheal and bronchial epithelial cell surfaces byMycoplasma pulmonis, submucosal and intraluminal immune and inflammatory cells, and altered airway activity. To determine the direct effect ofM. pulmonisupon transepithelial ion transport in the absence of immune and inflammatory cell responses, primary mouse tracheal epithelial cell monolayers (MTEs) were apically infected and assayed in Ussing chambers.M. pulmonis-infected MTEs, but not those infected with a nonmurine mycoplasma, demonstrated reductions in amiloride-sensitive Na+absorption, cyclic AMP, and cholinergic-stimulated Cl−secretion and transepithelial resistance. These effects were shown to require interaction of viable organisms with the apical surface of the monolayer and to be dependent upon organism number and duration of infection. Altered transport due toM. pulmoniswas not merely a result of epithelial cell death as evidenced by the following: (i) active transport of Na+and Cl−, albeit at reduced rates; (ii) normal cell morphology, including intact tight junctions, as demonstrated by electron microscopy; (iii) maintenance of a mean transepithelial resistance of 440 Ω/cm2; and (iv) lack of leakage of fluid from the basolateral to the apical surface of the monolayer. Alteration in epithelial ion transport in vitro is consistent with impaired pulmonary clearance and altered airway function inM. pulmonis-infected animals. Furthermore, the ability ofM. pulmonisto alter transport without killing the host cell may explain its successful parasitism and long-term persistence in the host. Further study of the MTE-M. pulmonismodel should elucidate the molecular mechanisms which mediate this reduction in transepithelial ion transport.