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Journal of Biological Regulators and Homeostatic Agents/Journal of Biological Regulators & Homeostatic Agents· 2020

Induction of pro-inflammatory cytokines (IL-1 and IL-6) and lung inflammation by COVID-19: anti-inflammatory strategies.

Pio Conti

Short summary

COVID-19 infection triggers pro-inflammatory cytokines IL-1β and IL-6, leading to lung inflammation, fever, and fibrosis via TLR and inflammasome activation. The novel cytokines IL-37 and IL-38 suppress these inflammatory pathways, presenting potential therapeutic strategies.

AI-generated from the title and abstract; the full text is not read.

Key points

  • COVID-19 infection activates TLRs and inflammasomes, leading to IL-1β and IL-6 release and subsequent lung inflammation.
  • IL-1β is a key mediator of lung inflammation, fever, and fibrosis in COVID-19.
  • IL-37 suppresses innate and acquired immune responses by inhibiting IL-1β, IL-6, TNF, and CCL2 via mTOR and AMP kinase pathways.
  • IL-38, another IL-1 family member, also suppresses IL-1β and other pro-inflammatory cytokines, offering therapeutic potential.

AI-generated from the title and abstract; the full text is not read.

Abstract

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.

The authors' abstract, as published at the source. Journal of Biological Regulators and Homeostatic Agents/Journal of Biological Regulators & Homeostatic Agents, 2020 · DOI ↗

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Field: Pharmacology (Medicine)

PharmacologyMedicine