SARS-CoV-2 is a type of beta-CoV that develops acute pneumonia, which is an inflammatory condition. A cytokine storm has been recognized as one of the leading causes of death in patients with COVID-19. ALI and ARDS along with multiple organ failure have also been presented as the consequences of acute inflammation and cytokine storm. It has been previously confirmed that SARS-CoV, as another member of the beta-CoV family, activates NLRP3 inflammasome and consequently develops acute inflammation in a variety of ways through having complex interactions with the host immune system using structural and nonstructural proteins. Numerous studies conducted on Tranilast have further demonstrated that the given drug can act as an effective anti-chemotactic factor on controlling inflammation, and thus, it can possibly help the improvement of the acute form of COVID-19 by inhibiting some key inflammation-associated transcription factors such as NF-κB and impeding NLRP3 inflammasome. Several studies have comparably revealed the direct effect of this drug on the prevention of inappropriate tissue’s remodeling; inhibition of neutrophils, IL-5, and eosinophils; repression of inflammatory cell infiltration into inflammation site; restriction of factors involved in acute airway inflammation like IL-33; and suppression of cytokine IL-13, which increase mucosal secretions. Therefore, Tranilast may be considered as a potential treatment for patients with the acute form of COVID-19 along with other drugs.

Interleukin (IL)‐22 is a member of IL‐10 family cytokines with various immunologic functions. As its name implies, IL‐22 is known to be secreted mainly by Th22 cells, a recently discovered lineage of CD4+ T cells. Also, Th17, Th1, natural killer cells, γδT cells, and innate immune cells along with some nonlymphoid cells have been confirmed as secondary cellular sources of IL‐22. Different cell types such as bronchial and intestinal epithelial cells, keratinocytes, hepatocytes, dermal fibroblasts, and tubular epithelial cells are affected by IL‐22. Both pathologic and protective roles have been attributed to IL‐22 in maintaining gut homeostasis and inflammation. According to the latest fast‐growing investigations, IL‐22 is significantly involved in various pathologies including allergic diseases, infection, autoimmunity, and cancer development. Regulating gut immune responses, barrier integrity, and inflammation is dependent on a diverse complex of cytokines and mediators which are secreted by mucosal immune cells. Several investigations have been designed to recognize the role of IL‐22 in gastrointestinal immunity. This article tries to discuss the latest knowledge on this issue and clarify the potential of IL‐22 to be used in the future therapeutic approaches of intestinal disorders including inflammatory bowel diseases and colon cancer.

Millions of people around the world are involved with COVID-19 due to infection with SARS-CoV-2. Virological features of SARS-CoV-2, including its genomic sequence, have been identified but the mechanisms governing COVID-19 immunopathogenesis have remained uncertain. miR-223 is a hematopoietic cell-derived miRNA that is implicated in regulating monocyte-macrophage differentiation, neutrophil recruitment, and pro-inflammatory responses. The miR-223 controls inflammation by targeting a variety of factors, including TRAF6, IKKα, HSP-70, FOXO1, TLR4, PI3K/AKT, PARP-1, HDAC2, ITGB3, CXCL2, CCL3, IL-6, IFN-I, STMN1, IL-1β, IL-18, Caspase-1, NF-κB, and NLRP3. The key role of miR-223 in regulating the inflammatory process and its antioxidant and antiviral role can suggest this miRNA as a potential regulatory factor in the process of COVID-19 immunopathogenesis.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has infected more than 126 million people worldwide and deaths exceed two million. Virological features of SARS-CoV-2, including its genomic sequence, have been identified but the mechanisms governing coronavirus disease 2019 (COVID-19) immunopathogenesis have remained uncertain. Severe COVID-19 is associated with a cytokine storm, chronic inflammation, neutrophilia, lymphocyte dysfunction, lymphopenia, reduction in T-lymphocytes and natural killer (NK) cells, disruption in viral clearance, and neutrophil/macrophage infiltration in the lungs. In many cases, patients develop acute lung injury (ALI), acute respiratory distress syndrome (ARDS), and/or multiple-organ dysfunction syndrome (MODS). Resveratrol reduces the expression of inflammasome activators such as thioredoxin-interacting protein (TXNIP) and nuclear factor erythroid 2 (NrF2) and increases that of the inflammasome inhibitor, i.e., NAD-dependent deacetylase sirtuin-1 (SIRT1). Resveratrol is able to inhibit the production of reactive oxygen species (ROS) and the activation of inducible nitric oxide synthases (iNOS). It affects signaling pathways including mitogen-activated protein kinase (MAPK) and nuclear factor kappa B (NF-ĸB) thereby further inhibiting inflammasomes. Because of its anti-inflammasome, anti-inflammatory, and anti-oxidant effects and considering the key role of inflammation and cytokine storm in disease severity and poor patient outcomes, it is concluded that resveratrol can be useful in the treatment of COVID-19. Given the persistence of the COVID-19 pandemic and the challenges of extensive vaccination in all countries, it is important to achieve more effective treatments to decrease the mortality rate and severity of severe injuries following COVID-19. Given all the effects reviewed in this article, resveratrol at a dose of up to 600 mg per day can be exploited as a potential adjunctive therapy for COVID-19 patients.