Basheer Maamoun, Saad Elias, Kananeh Majd, Asad Layyous, Khayat Osama, Badarne Anan, Abdo Zaki, Arraf Nada, Milhem Faris, Bassal Tamara, Boulos Mariana, Assy Nimer
Internal Medicine Department A, Galilee Medical Center, Nahariya 221001, Israel.
The Azrieli Faculty of Medicine, Bar-Ilan University, Safad 1311502, Israel.
Curr Issues Mol Biol. 2022 Oct 10;44(10):4735-4747. doi: 10.3390/cimb44100323.
(1) Background/Aim: People infected with SARS-CoV-2 may develop COVID-19 in a wide range of clinical severity. Pulmonary fibrosis is characterized by several grades of chronic inflammation and collagen deposition in the interalveolar space. SARS-CoV-2 infection has been demonstrated to cause lung fibrosis without a currently elucidated mechanism. Some studies emphasize the role of proinflammatory cytokines. This research studies the correlation of the released cytokines with mortality or lung injury in COVID-19 patients. (2) Methods: Electronic medical record data from 40 patients diagnosed with COVID-19 in the COVID-19 Department, Galilee Medical Center, Nahariya, Israel, were collected. Epidemiological, clinical, laboratory, and imaging variables were analyzed. The cytokine levels were measured upon admission and discharge. A correlation between cytokine levels and severity and mortality or lung involvement was undertaken. (3) Results: IFN-gamma and IL-10 are the most powerful risk factors for mortality in the COVID-19 patient groups in a multivariate analysis. However, in a univariate analysis, TGF-β, CXCL-10, IFN gamma, and IL-7 affected mortality in COVID-19 patients. MMP-7 was significantly correlated with a cytokine storm and a high 4-C (severity) score in COVID-19 patients. MMP-7, TGF-β, IL-10, IL-7, TNF-α, and IL-6 were correlated with high lung involvement in COVID-19 patients. Serum concentrations of IGF-1 were significantly increased upon discharge, but MMP-7 was decreased. (4) Conclusions: Proinflammatory cytokines predict clinical severity, lung fibrosis, and mortality in COVID-19 patients. High concentrations of TGF-β, CXCL-10, IL-10, IL-6, and TNF-α are correlated to severity and lung injury. However, certain cytokines have protective effects and higher levels of these cytokines increase survival levels and lower lung damage. High levels of INF-γ, IL-7, MMP-7, and IGF-1 have protection probabilities against lung injury and severity.
(1) 背景/目的:感染严重急性呼吸综合征冠状病毒2(SARS-CoV-2)的人可能会发展出临床严重程度各异的新型冠状病毒肺炎(COVID-19)。肺纤维化的特征是肺泡间隙存在不同程度的慢性炎症和胶原蛋白沉积。已证实SARS-CoV-2感染可导致肺纤维化,但其机制目前尚不清楚。一些研究强调促炎细胞因子的作用。本研究探讨COVID-19患者中释放的细胞因子与死亡率或肺损伤的相关性。(2) 方法:收集了以色列纳哈里亚加利利医疗中心COVID-19科40例确诊为COVID-19患者的电子病历数据。分析了流行病学、临床、实验室和影像学变量。在入院和出院时测量细胞因子水平。研究了细胞因子水平与严重程度、死亡率或肺部受累情况之间的相关性。(3) 结果:在多变量分析中,干扰素-γ(IFN-γ)和白细胞介素-10(IL-10)是COVID-19患者组中死亡率的最强风险因素。然而,在单变量分析中,转化生长因子-β(TGF-β)、CXC趋化因子配体10(CXCL-10)、干扰素-γ和白细胞介素-7(IL-7)影响COVID-19患者的死亡率。基质金属蛋白酶-7(MMP-7)与COVID-19患者的细胞因子风暴和高4-C(严重程度)评分显著相关。MMP-7、TGF-β、IL-10、IL-7、肿瘤坏死因子-α(TNF-α)和白细胞介素-6与COVID-19患者的高肺部受累情况相关。出院时胰岛素样生长因子-1(IGF-1)的血清浓度显著升高,但MMP-7降低。(4) 结论:促炎细胞因子可预测COVID-19患者的临床严重程度、肺纤维化和死亡率。高浓度的TGF-β、CXCL-10、IL-10、IL-6和TNF-α与严重程度和肺损伤相关。然而,某些细胞因子具有保护作用,这些细胞因子水平较高可提高生存率并降低肺损伤。高水平的干扰素-γ、IL-7、MMP-7和IGF-1具有预防肺损伤和严重程度的可能性。