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脂肪基质细胞浓缩分泌组限制小鼠流感病毒诱导的肺损伤。

Concentrated Secretome of Adipose Stromal Cells Limits Influenza A Virus-Induced Lung Injury in Mice.

机构信息

Division of Pulmonary, Critical Care and Sleep, Department of Medicine, Indiana University School of Medicine, Indianapolis, IN 46202, USA.

Theratome Bio, Inc., Indianapolis, IN 46202, USA.

出版信息

Cells. 2021 Mar 24;10(4):720. doi: 10.3390/cells10040720.

Abstract

Despite vaccination and antivirals, influenza remains a communicable disease of high burden, with limited therapeutic options available to patients that develop complications. Here, we report the development and preclinical characterization of Adipose Stromal Cell (ASC) concentrated secretome (CS), generated by process adaptable to current Good Manufacturing Practices (cGMP) standards. We demonstrate that ASC-CS limits pulmonary histopathological changes, infiltration of inflammatory cells, protein leak, water accumulation, and arterial oxygen saturation (spO2) reduction in murine model of lung infection with influenza A virus (IAV) when first administered six days post-infection. The ability to limit lung injury is sustained in ASC-CS preparations stored at -80 °C for three years. Priming of the ASC with inflammatory factors TNFα and IFNγ enhances ASC-CS ability to suppress lung injury. IAV infection is associated with dramatic increases in programmed cell death ligand (PDL1) and angiopoietin 2 (Angpt2) levels. ASC-CS application significantly reduces both PDL1 and Angpt2 levels. Neutralization of PDL1 with anti-mouse PDL1 antibody starting Day6 onward effectively ablates lung PDL1, but only non-significantly reduces Angpt2 release. Most importantly, late-phase PDL1 neutralization results in negligible suppression of protein leakage and inflammatory cell infiltration, suggesting that suppression of PDL1 does not play a critical role in ASC-CS therapeutic effects.

摘要

尽管有疫苗和抗病毒药物,流感仍然是一种具有高负担的传染病,对于出现并发症的患者,可用的治疗选择有限。在这里,我们报告了脂肪基质细胞(ASC)浓缩分泌液(CS)的开发和临床前特征,该分泌液是通过可适应现行良好生产规范(cGMP)标准的工艺产生的。我们证明,在感染流感病毒(IAV)的小鼠模型中,ASC-CS 可在感染后六天首次给药时限制肺部组织病理学变化、炎症细胞浸润、蛋白渗漏、水分积聚和动脉血氧饱和度(spO2)降低。在 -80°C 下储存三年的 ASC-CS 制剂仍具有限制肺损伤的能力。用炎性因子 TNFα 和 IFNγ 对 ASC 进行预处理可增强 ASC-CS 抑制肺损伤的能力。IAV 感染与程序性细胞死亡配体 1(PDL1)和血管生成素 2(Angpt2)水平的显著增加相关。ASC-CS 的应用可显著降低 PDL1 和 Angpt2 水平。从第 6 天开始用抗小鼠 PDL1 抗体中和 PDL1 可有效耗尽肺部 PDL1,但仅能非显著地降低 Angpt2 的释放。最重要的是,晚期 PDL1 中和几乎不能抑制蛋白渗漏和炎症细胞浸润,表明抑制 PDL1 不会在 ASC-CS 的治疗效果中发挥关键作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/70ef/8063825/1c94c942eb01/cells-10-00720-g001.jpg

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