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首页> 外文期刊>American Journal of Physiology >Nucleotide-mediated inhibition of alveolar fluid clearance in BALB/c mice after respiratory syncytial virus infection.
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Nucleotide-mediated inhibition of alveolar fluid clearance in BALB/c mice after respiratory syncytial virus infection.

机译：呼吸道合胞病毒感染后，核苷酸介导的BALB / c小鼠肺泡液清除的抑制作用。

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摘要

Respiratory syncytial virus (RSV) is the most common cause of lower respiratory tract disease in infants and children worldwide. Intranasal infection of BALB/c mice with RSV strain A2, but not ultraviolet-inactivated RSV, for 2 or 4 days reduced basal alveolar fluid clearance (AFC), a seminal function of bronchoalveolar epithelium, and caused loss of AFC sensitivity to amiloride inhibition. Reduced AFC was temporally associated with increased lung water content but was not a consequence of increased epithelial permeability or cell death. Reduced AFC was also not due to decreased transcription of epithelial Na+ channel subunit genes in lung tissue. RSV-mediated inhibition of AFC 2 days after infection was rapidly prevented by addition to the instillate of P2Y receptor antagonists (suramin and XAMR-0721) or enzymes that degrade UTP, but not those that degrade ATP. After UTP degradation, AFC returned to control levels but was no longer sensitive to amiloride. UTP at nanomolar concentrations recapitulated the AFC inhibitory effect of RSV in normal mice and mice infected with RSV for 6 days, indicating that normalization of AFC at this time point is a consequence of cessation of UTP release, rather than P2Y receptor desensitization. We conclude that RSV infection of the bronchoalveolar epithelium results in reduced AFC as a consequence of autocrine feedback inhibition mediated by UTP. These studies are the first to demonstrate AFC inhibition by an important pulmonary viral pathogen. Reduced AFC may result in formation of an increased volume of fluid mucus, airway congestion, and rhinorrhea, all features of severe RSV disease.
机译：呼吸道合胞病毒（RSV）是全世界婴儿和儿童下呼吸道疾病的最常见原因。用RSV毒株A2对BALB / c小鼠进行鼻内感染，但不对紫外线灭活的RSV进行2或4天的鼻内感染，减少了基础肺泡液清除率（AFC），支气管肺泡上皮的主要功能，并导致AFC对阿米洛利抑制的敏感性降低。 AFC减少在时间上与肺水含量增加有关，但不是上皮通透性增加或细胞死亡的结果。 AFC的减少也不是由于肺组织中上皮Na +通道亚基基因的转录减少所致。通过添加P2Y受体拮抗剂（苏拉明和XAMR-0721）或降解UTP的酶（而不是降解ATP的酶），可迅速预防RSV介导的感染后2天对AFC的抑制。 UTP降解后，AFC恢复至控制水平，但对阿米洛利不再敏感。纳摩尔浓度的UTP在正常小鼠和感染RSV 6天的小鼠中概括了RSV对AFC的抑制作用，表明此时AFC的正常化是停止UTP释放而不是P2Y受体脱敏的结果。我们得出结论，由于UTP介导的自分泌反馈抑制，支气管肺泡上皮的RSV感染导致AFC减少。这些研究首次证明了重要的肺病毒病原体对AFC的抑制作用。减少的AFC可能导致形成大量的液体粘液，气道充血和鼻漏，这是严重RSV疾病的所有特征。

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