Rabaan Ali A, Al-Ahmed Shamsah H, Muhammad Javed, Khan Amjad, Sule Anupam A, Tirupathi Raghavendra, Mutair Abbas Al, Alhumaid Saad, Al-Omari Awad, Dhawan Manish, Tiwari Ruchi, Sharun Khan, Mohapatra Ranjan K, Mitra Saikat, Bilal Muhammad, Alyami Salem A, Emran Talha Bin, Moni Mohammad Ali, Dhama Kuldeep
Molecular Diagnostic Laboratory, Johns Hopkins Aramco Healthcare, Dhahran 31311, Saudi Arabia.
Specialty Paediatric Medicine, Qatif Central Hospital, Qatif 32654, Saudi Arabia.
Vaccines (Basel). 2021 Apr 29;9(5):436. doi: 10.3390/vaccines9050436.
Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is a severe pandemic of the current century. The vicious tentacles of the disease have been disseminated worldwide with unknown complications and repercussions. Advanced COVID-19 syndrome is characterized by the uncontrolled and elevated release of pro-inflammatory cytokines and suppressed immunity, leading to the cytokine storm. The uncontrolled and dysregulated secretion of inflammatory and pro-inflammatory cytokines is positively associated with the severity of the viral infection and mortality rate. The secretion of various pro-inflammatory cytokines such as TNF-α, IL-1, and IL-6 leads to a hyperinflammatory response by recruiting macrophages, T and B cells in the lung alveolar cells. Moreover, it has been hypothesized that immune cells such as macrophages recruit inflammatory monocytes in the alveolar cells and allow the production of large amounts of cytokines in the alveoli, leading to a hyperinflammatory response in severely ill patients with COVID-19. This cascade of events may lead to multiple organ failure, acute respiratory distress, or pneumonia. Although the disease has a higher survival rate than other chronic diseases, the incidence of complications in the geriatric population are considerably high, with more systemic complications. This review sheds light on the pivotal roles played by various inflammatory markers in COVID-19-related complications. Different molecular pathways, such as the activation of JAK and JAK/STAT signaling are crucial in the progression of cytokine storm; hence, various mechanisms, immunological pathways, and functions of cytokines and other inflammatory markers have been discussed. A thorough understanding of cytokines' molecular pathways and their activation procedures will add more insight into understanding immunopathology and designing appropriate drugs, therapies, and control measures to counter COVID-19. Recently, anti-inflammatory drugs and several antiviral drugs have been reported as effective therapeutic drug candidates to control hypercytokinemia or cytokine storm. Hence, the present review also discussed prospective anti-inflammatory and relevant immunomodulatory drugs currently in various trial phases and their possible implications.
2019冠状病毒病(COVID-19)由严重急性呼吸综合征冠状病毒2(SARS-CoV-2)引起,是本世纪的一场严重大流行疾病。该疾病的恶性触角已蔓延至全球,其并发症和影响尚不明朗。重症COVID-19综合征的特征是促炎细胞因子不受控制地过度释放以及免疫力受到抑制,从而导致细胞因子风暴。炎症和促炎细胞因子不受控制且失调的分泌与病毒感染的严重程度和死亡率呈正相关。多种促炎细胞因子如肿瘤坏死因子-α、白细胞介素-1和白细胞介素-6的分泌通过在肺泡细胞中募集巨噬细胞、T细胞和B细胞导致过度炎症反应。此外,据推测,巨噬细胞等免疫细胞会在肺泡细胞中募集炎性单核细胞,并使肺泡中产生大量细胞因子,从而导致COVID-19重症患者出现过度炎症反应。这一系列事件可能导致多器官功能衰竭、急性呼吸窘迫或肺炎。尽管该疾病的生存率高于其他慢性疾病,但老年人群中的并发症发生率相当高,且有更多的全身并发症。本综述揭示了各种炎症标志物在COVID-19相关并发症中所起的关键作用。不同的分子途径,如JAK和JAK/STAT信号通路的激活在细胞因子风暴的进展中至关重要;因此,本文讨论了细胞因子和其他炎症标志物的各种机制、免疫途径及功能。深入了解细胞因子的分子途径及其激活过程将有助于更深入地理解免疫病理学,并设计出合适的药物、疗法和控制措施来对抗COVID-19。最近,抗炎药物和几种抗病毒药物已被报道为控制高细胞因子血症或细胞因子风暴的有效治疗候选药物。因此,本综述还讨论了目前处于不同试验阶段的前瞻性抗炎和相关免疫调节药物及其可能的影响。