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循环中较低水平的干扰素-γ是 COVID-19 患者肺纤维化的一个风险因素。

Lower Circulating Interferon-Gamma Is a Risk Factor for Lung Fibrosis in COVID-19 Patients.

机构信息

Beijing Youan Hospital, Capital Medical University, Beijing, China.

Department of Immunology, Centre for Immunotherapy, Institute of Basic Medical Sciences, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, China.

出版信息

Front Immunol. 2020 Sep 29;11:585647. doi: 10.3389/fimmu.2020.585647. eCollection 2020.

DOI:10.3389/fimmu.2020.585647
PMID:33133104
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7550399/
Abstract

Cytokine storm resulting from SARS-CoV-2 infection is one of the leading causes of acute respiratory distress syndrome (ARDS) and lung fibrosis. We investigated the effect of inflammatory molecules to identify any marker that is related to lung fibrosis in coronavirus disease 2019 (COVID-19). Seventy-six COVID-19 patients who were admitted to Youan Hospital between January 21 and March 20, 2020 and recovered were recruited for this study. Pulmonary fibrosis, represented as fibrotic volume on chest CT images, was computed by an artificial intelligence (AI)-assisted program. Plasma samples were collected from the participants shortly after admission, to measure the basal inflammatory molecules levels. At discharge, fibrosis was present in 46 (60.5%) patients whose plasma interferon-γ (IFN-γ) levels were twofold lower than those without fibrosis ( > 0.05). The multivariate-adjusted logistic regression analysis demonstrated the inverse association risk of having lung fibrosis and basal circulating IFN-γ levels with an estimate of 0.43 ( = 0.02). Per the 1-SD increase of basal IFN-γ level in circulation, the fibrosis volume decreased by 0.070% ( = 0.04) at the discharge of participants. The basal circulating IFN-γ levels were comparable with c-reactive protein in the discrimination of the occurrence of lung fibrosis among COVID-19 patients at discharge, unlike circulating IL-6 levels. In conclusion, these data indicate that decreased circulating IFN-γ is a risk factor of lung fibrosis in COVID-19.

摘要

SARS-CoV-2 感染引起的细胞因子风暴是急性呼吸窘迫综合征(ARDS)和肺纤维化的主要原因之一。我们研究了炎症分子的作用,以确定与 2019 冠状病毒病(COVID-19)相关的肺纤维化标志物。2020 年 1 月 21 日至 3 月 20 日期间,我们招募了 76 名在佑安医院住院并康复的 COVID-19 患者。通过人工智能(AI)辅助程序计算胸部 CT 图像上的纤维化体积来表示肺纤维化。入院后不久,从参与者中采集血浆样本,以测量基础炎症分子水平。出院时,46 名(60.5%)患者存在纤维化,其血浆干扰素-γ(IFN-γ)水平比无纤维化患者低两倍(>0.05)。多变量调整的逻辑回归分析表明,肺纤维化和基础循环 IFN-γ水平与风险呈反比,估计值为 0.43(=0.02)。基础循环 IFN-γ水平每增加 1-SD,参与者出院时纤维化体积减少 0.070%(=0.04)。在区分 COVID-19 患者出院时肺纤维化的发生方面,基础循环 IFN-γ水平与 C 反应蛋白相当,而与循环 IL-6 水平不同。总之,这些数据表明,循环 IFN-γ降低是 COVID-19 肺纤维化的危险因素。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7fc7/7550399/e1e3a1bde816/fimmu-11-585647-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7fc7/7550399/fd69ab9dbc98/fimmu-11-585647-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7fc7/7550399/62f4c4ae540b/fimmu-11-585647-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7fc7/7550399/6035ab59104a/fimmu-11-585647-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7fc7/7550399/e1e3a1bde816/fimmu-11-585647-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7fc7/7550399/fd69ab9dbc98/fimmu-11-585647-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7fc7/7550399/62f4c4ae540b/fimmu-11-585647-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7fc7/7550399/6035ab59104a/fimmu-11-585647-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7fc7/7550399/e1e3a1bde816/fimmu-11-585647-g004.jpg

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