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人博卡病毒引起的肺部感染在体内和体外均可诱导促纤维化介质细胞因子的释放。

Lung Infection by Human Bocavirus Induces the Release of Profibrotic Mediator Cytokines In Vivo and In Vitro.

作者信息

Khalfaoui Soumaya, Eichhorn Vivien, Karagiannidis Christian, Bayh Inga, Brockmann Michael, Pieper Monika, Windisch Wolfram, Schildgen Oliver, Schildgen Verena

机构信息

Kliniken der Stadt Köln gGmbH, University Hospital Witten/Herdecke, Cologne-Merheim, Ostmerheimer Strasse 200, Institute for Pathology, D-51109 Cologne, Germany.

Kliniken der Stadt Köln gGmbH, University Hospital Witten/Herdecke, Cologne-Merheim, Ostmerheimer Strasse 200, Department of Pneumology and Critical Care Medicine, D-51109 Cologne, Germany.

出版信息

PLoS One. 2016 Jan 25;11(1):e0147010. doi: 10.1371/journal.pone.0147010. eCollection 2016.

Abstract

Human Bocavirus subtype 1 (HBoV1) is associated with respiratory diseases and may contribute to chronic lung diseases by persisting in the infected host. Here the question was addressed if HBoV infections could contribute to fibrogenesis processes as suggested by previously published clinical observations. Cytokine profiles induced by HBoV infection in CuFi-8 air-liquid interphase cell cultures and in bronchoalveolar lavage fluid (BALF) of 20 HBoV-positive and 12 HBoV-negative patients were analysed by semi-quantitative Western spot blot analyses. Although lots of cytokines were regulated independently of HBoV status, several cytokines associated with lung fibrosis and tumour development, e.g., EGF, VEGF, TARC (CCL17), TNF-α, TNF-β, TIMP-1, were clearly upregulated in the HBoV-positive cohort. These findings suggest that the development of lung fibrosis might be triggered by HBoV induced cytokine expression.

摘要

人博卡病毒1型(HBoV1)与呼吸道疾病有关,并且可能通过在受感染宿主中持续存在而导致慢性肺部疾病。此前发表的临床观察结果表明HBoV感染可能促成纤维化过程,在此对这一问题进行了研究。通过半定量蛋白质免疫印迹分析,对CuFi-8气液界面细胞培养物以及20例HBoV阳性和12例HBoV阴性患者的支气管肺泡灌洗液(BALF)中HBoV感染诱导的细胞因子谱进行了分析。尽管许多细胞因子的调节与HBoV状态无关,但在HBoV阳性队列中,几种与肺纤维化和肿瘤发展相关的细胞因子,如表皮生长因子(EGF)、血管内皮生长因子(VEGF)、胸腺和活化调节趋化因子(TARC,即CCL17)、肿瘤坏死因子-α(TNF-α)、肿瘤坏死因子-β(TNF-β)、金属蛋白酶组织抑制因子-1(TIMP-1)明显上调。这些发现表明,肺纤维化的发展可能由HBoV诱导的细胞因子表达引发。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b64/4726461/d15ea95be566/pone.0147010.g001.jpg

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