Evaluating the Role of the Interleukin-23/17 Axis in Critically Ill COVID-19 Patients.

Evaluating the Role of the Interleukin-23/17 Axis in Critically Ill COVID-19 Patients.
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评估白介素-23/17轴在危重患病患者中的作用。

DOI:
10.3390/jpm11090891
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发表时间:
2021-09-07
影响因子:
--
通讯作者:
Kotanidou A
Kotanidou A
中科院分区:
医学4区
文献类型:
--
作者:
Jahaj E;Vassiliou AG;Keskinidou C;Gallos P;Vrettou CS;Tsipilis S;Mastora Z;Orfanos SE;Dimopoulou I;Kotanidou A

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研究假设白细胞介素(IL)-23/17轴在2019冠状病毒病(COVID-19)中的潜在作用。然而,迄今为止,尚未在重症COVID-19患者和重症非COVID-19患者之间比较IL-23和IL-17的水平。在重症COVID-19(N = 38)和重症非COVID-19(N = 34)患者(危重疾病严重程度相同)入住重症监护室(ICU)时测量IL-23和IL-17。重症非COVID-19患者在ICU入院时未发生败血症或感染性休克。入组患者既往均未接受过皮质类固醇。在我们的研究中,COVID-19患者的循环IL-17水平较高。更具体地说,重症COVID-19患者的水平为0.78(0.05-1.8)pg/mL,而重症非COVID-19患者为0.11(0.05-0.9)pg/mL(p = 0.04)。相比之下,组间IL-23水平相当。一组在专门的COVID-19诊所住院的患者(N = 16)也用于评估IL-17和IL-23水平与COVID-19严重程度的关系。非重症COVID-19患者的两种细胞因子水平均检测不到。我们的结果支持在严重COVID-19感染中抑制IL-17的概念。
Studies have hypothesized a potential role of the interleukin (IL)-23/17 axis in coronavirus disease 2019 (COVID-19). However, to date, levels of IL-23 and 17 have not been compared between critically ill COVID-19 patients and critically ill non-COVID-19 patients. IL-23 and 17 were measured on admission to the intensive care unit (ICU) in critically ill COVID-19 (N = 38) and critically ill non-COVID-19 (N = 34) patients with an equal critical illness severity. Critically ill non-COVID-19 patients did not have sepsis or septic shock on ICU admission. None of the enrolled patients had previously received corticosteroids. In our study, circulating IL-17 levels were higher in the COVID-19 patients. More specifically, critically ill COVID-19 patients had levels of 0.78 (0.05–1.8) pg/mL compared to 0.11 (0.05–0.9) pg/mL in the critically ill non-COVID-19 patients (p = 0.04). In contrast, IL-23 levels were comparable between groups. A group of patients hospitalized in the specialized COVID-19 clinic (N = 16) was also used to evaluate IL-17 and IL-23 levels with respect to COVID-19 severity. Non-critically ill COVID-19 patients had undetectable levels of both cytokines. Our results support the notion of inhibiting IL-17 in critical COVID-19 infection.
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