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李冬, 王凤杰, 余磊, 姚文荣, 崔艳芳, 杨贵波. 2017: SHIV/SIV感染恒河猴气管粘膜中pIgR的表达. 动物学研究, 38(1): 44-48. DOI: 10.13918/j.issn.2095-8137.2017.007
引用本文: 李冬, 王凤杰, 余磊, 姚文荣, 崔艳芳, 杨贵波. 2017: SHIV/SIV感染恒河猴气管粘膜中pIgR的表达. 动物学研究, 38(1): 44-48. DOI: 10.13918/j.issn.2095-8137.2017.007
Dong Li, Feng-Jie Wang, Lei Yu, Wen-Rong Yao, Yan-Fang Cui, Gui-Bo Yang. 2017. Expression of pIgR in the tracheal mucosa of SHIV/SIV-infected rhesus macaques. Zoological Research, 38(1): 44-48. DOI: 10.13918/j.issn.2095-8137.2017.007
Citation: Dong Li, Feng-Jie Wang, Lei Yu, Wen-Rong Yao, Yan-Fang Cui, Gui-Bo Yang. 2017. Expression of pIgR in the tracheal mucosa of SHIV/SIV-infected rhesus macaques. Zoological Research, 38(1): 44-48. DOI: 10.13918/j.issn.2095-8137.2017.007

SHIV/SIV感染恒河猴气管粘膜中pIgR的表达

Expression of pIgR in the tracheal mucosa of SHIV/SIV-infected rhesus macaques

  • 摘要: 多聚免疫球蛋白受体(pIgR)参与分泌型IgA(S-IgA)的形成和分泌,在预防呼吸系统微生物感染和定植中具有重要作用。尽管在HIV/AIDS中微生物感染和定植增加是普遍现象,但关于这些患者呼吸道粘膜pIgR表达的研究几无报道。为此,本文利用实时荧光定量PCR和激光扫描共聚焦显微镜对SHIV/SIV感染恒河猴气管粘膜和肺中pIgR的表达进行了观察。发现SHIV/SIV感染恒河猴气管粘膜中pIgR mRNA和pIgR免疫反应性的水平低于未感染恒河猴;能够调节pIgR表达的IL-17A的水平也发生了相似的变化。肺中的变化与气管不同,感染恒河猴pIgR与IL-17A的表达水平高于正常个体。这些结果表明pIgR表达在SHIV/SIV感染,并可能在HIV感染后出现异常,可能部分地由IL-17A的改变所致。这些变化可能与HIV/AIDS患者呼吸系统并发症相关的微生物感染和定植增加有关。

     

    Abstract: Polymeric immunoglobulin receptors(pIgR) are key participants in the formation and secretion of secretory IgA(S-IgA), which is critical for the prevention of microbial infection and colonization in the respiratory system. Although increased respiratory colonization and infections are common in HIV/AIDS, little is known about the expression of pIgR in the airway mucosa of these patients. To address this, the expression levels of pIgR in the tracheal mucosa and lungs of SHIV/SIV-infected rhesus macaques were examined by real-time RTPCR and confocal microscopy. We found that the levels of both PIGR mRNA and pIgR immunoreactivity were lower in the tracheal mucosa of SHIV/SIV-infected rhesus macaques than that in non-infected rhesus macaques, and the difference in pIgR immunoreactivity was statistically significant. IL-17A, which enhances pIgR expression, was also changed in the same direction as that of pIgR. In contrast to changes in the tracheal mucosa, pIgR and IL-17A levels were higher in the lungs of infected rhesus macaques. These results indicated abnormal pIgR expression in SHIV/SIV, and by extension HIV infections, which might partially result from IL-17A alterations and might contribute to the increased microbial colonization and infection related to pulmonary complications in HIV/AIDS.

     

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