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引起 COVID-19 的 SARS-CoV-2 可导致儿童川崎病:促炎和抗炎细胞因子的作用。

SARS-CoV-2, which induces COVID-19, causes kawasaki-like disease in children: role of pro-inflammatory and anti-inflammatory cytokines.

机构信息

Clinica dei Pazienti del Territorio, Fondazione Policlinico Gemelli, Rome, Italy.

Specialization School in Oral Surgery, Vita-Salute San Raffaele University, Milan, Italy.

出版信息

J Biol Regul Homeost Agents. 2020;34(3):767-773. doi: 10.23812/EDITORIAL-RONCONI-E-59.

Abstract

Acute severe respiratory syndrome coronavirus-2 (SARS-CoV-2) caused a global pandemic coronavirus disease 2019 (COVID-19). In humans, SARS-CoV-2 infection leads to acute respiratory distress syndrome which presents edema, hemorrhage, intra-alveolar fibrin deposition, and vascular changes characterized by thrombus formation, micro-angiopathy and thrombosis. These clinical signs are mediated by pro-inflammatory cytokines. In recent studies it has been noted that COVID-19 pandemic can affect patients of all ages, including children (even if less severely) who were initially thought to be immune. Kawasaki disease is an autoimmune acute febrile inflammatory condition, which primarily affects young children. The disease can present immunodeficiency with the inability of the immune system to fight inflammatory pathogens and leads to fever, rash, alterations of the mucous membranes, conjunctiva infection, pharyngeal erythema, adenopathy, and inflammation. In the COVID-19 period, virus infection aggravates the condition of Kawasaki disease, but it has also been noted that children affected by SARS-V-2 may develop a disease similar to Kawasaki's illness. However, it is uncertain whether the virus alone can give Kawasaki disease-like forms. As in COVID-19, Kawasaki disease and its similar forms are mediated by pro-inflammatory cytokines produced by innate immunity cells such as macrophages and mast cells (MCs). In light of the above, it is therefore pertinent to think that by blocking pro-inflammatory cytokines with new anti-inflammatory cytokines, such as IL-37 and IL-38, it is possible to alleviate the symptoms of the disease and have a new available therapeutic tool. However, since Kawasaki and Kawasaki-like diseases present immunodeficiency, treatment with anti-inflammatory/immunosuppressant molecules must be applied very carefully.

摘要

急性严重呼吸综合征冠状病毒 2 型(SARS-CoV-2)引发了全球大流行的 2019 年冠状病毒病(COVID-19)。在人类中,SARS-CoV-2 感染导致急性呼吸窘迫综合征,其表现为水肿、出血、肺泡内纤维蛋白沉积以及以血栓形成、微血管病和血栓形成为特征的血管变化。这些临床症状是由促炎细胞因子介导的。在最近的研究中,人们注意到 COVID-19 大流行可能会影响所有年龄段的患者,包括最初被认为具有免疫力的儿童(即使症状较轻)。川崎病是一种自身免疫性急性发热性炎症性疾病,主要影响幼儿。该疾病可能表现为免疫缺陷,即免疫系统无法抵抗炎症病原体,导致发热、皮疹、黏膜改变、结膜炎感染、咽部红斑、淋巴结病和炎症。在 COVID-19 期间,病毒感染会加重川崎病的病情,但也有研究指出,感染 SARS-CoV-2 的儿童可能会患上类似于川崎病的疾病。然而,尚不确定病毒是否单独可以引起类似于川崎病的疾病。与 COVID-19 一样,川崎病及其类似形式是由先天免疫细胞(如巨噬细胞和肥大细胞[MCs])产生的促炎细胞因子介导的。鉴于上述情况,因此可以认为,通过使用新的抗炎细胞因子(如 IL-37 和 IL-38)阻断促炎细胞因子,可以缓解疾病症状,并提供新的治疗手段。然而,由于川崎病和川崎病样疾病存在免疫缺陷,因此必须非常谨慎地应用抗炎/免疫抑制分子进行治疗。

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