Postgraduate Medical School, University of Chieti, Chieti, Italy.
Clinica dei Pazienti del Territorio, Fondazione Policlinico Gemelli, Rome, Italy.
J Biol Regul Homeost Agents. 2020;34(2):327-331. doi: 10.23812/CONTI-E.
Coronavirus-19 (COVI-19) involves humans as well as animals and may cause serious damage to the respiratory tract, including the lung: coronavirus disease (COVID-19). This pathogenic virus has been identified in swabs performed on the throat and nose of patients who suffer from or are suspected of the disease. When COVI-19 infect the upper and lower respiratory tract it can cause mild or highly acute respiratory syndrome with consequent release of pro-inflammatory cytokines, including interleukin (IL)-1β and IL-6. The binding of COVI-19 to the Toll Like Receptor (TLR) causes the release of pro-IL-1β which is cleaved by caspase-1, followed by inflammasome activation and production of active mature IL-1β which is a mediator of lung inflammation, fever and fibrosis. Suppression of pro-inflammatory IL-1 family members and IL-6 have been shown to have a therapeutic effect in many inflammatory diseases, including viral infections. Cytokine IL-37 has the ability to suppress innate and acquired immune response and also has the capacity to inhibit inflammation by acting on IL-18Rα receptor. IL-37 performs its immunosuppressive activity by acting on mTOR and increasing the adenosine monophosphate (AMP) kinase. This cytokine inhibits class II histocompatibility complex (MHC) molecules and inflammation in inflammatory diseases by suppressing MyD88 and subsequently IL-1β, IL-6, TNF and CCL2. The suppression of IL-1β by IL-37 in inflammatory state induced by coronavirus-19 can have a new therapeutic effect previously unknown. Another inhibitory cytokine is IL-38, the newest cytokine of the IL-1 family members, produced by several immune cells including B cells and macrophages. IL-38 is also a suppressor cytokine which inhibits IL-1β and other pro-inflammatory IL-family members. IL-38 is a potential therapeutic cytokine which inhibits inflammation in viral infections including that caused by coronavirus-19, providing a new relevant strategy.
新型冠状病毒（COVID-19）涉及人类和动物，可能会对包括肺部在内的呼吸道造成严重损害：冠状病毒病（COVID-19）。该病原体已在患有或疑似患有该疾病的患者的喉咙和鼻腔拭子中得到确认。当 COVI-19 感染上呼吸道和下呼吸道时，可能会导致轻度或高度急性呼吸综合征，从而导致促炎细胞因子的释放，包括白细胞介素（IL）-1β和 IL-6。COVI-19 与 Toll 样受体（TLR）结合会导致前 IL-1β 的释放，前 IL-1β 被半胱天冬酶-1 切割，随后激活炎症小体并产生活性成熟的 IL-1β，后者是肺部炎症、发热和纤维化的介质。在许多炎症性疾病（包括病毒感染）中，抑制促炎的 IL-1 家族成员和 IL-6 已显示出治疗效果。细胞因子 IL-37 具有抑制先天和获得性免疫反应的能力，并且通过作用于 IL-18Rα 受体也具有抑制炎症的能力。IL-37 通过作用于 mTOR 并增加单磷酸腺苷（AMP）激酶来发挥其免疫抑制活性。该细胞因子通过抑制 MyD88 并随后抑制 IL-1β、IL-6、TNF 和 CCL2 来抑制炎症性疾病中的 II 类主要组织相容性复合物（MHC）分子和炎症。IL-37 抑制冠状病毒-19 诱导的炎症状态下的 IL-1β 可能具有以前未知的新治疗效果。另一种抑制性细胞因子是 IL-38，它是 IL-1 家族成员的最新细胞因子，由包括 B 细胞和巨噬细胞在内的几种免疫细胞产生。IL-38 也是一种抑制性细胞因子，可抑制 IL-1β 和其他促炎 IL 家族成员。IL-38 是一种潜在的治疗性细胞因子，可抑制包括冠状病毒-19 在内的病毒感染引起的炎症，提供了一种新的相关策略。
