COVID-19'nin Pro-inflamatuar Sitokinlere (IL-1 ve IL-6) Neden Olduğu ve Anti-inflamatuar Stratejiler Olarak IL-37 ve IL-38
Induction of pro-inflammatory cytokines (IL-1 and IL-6) and lung inflammation by COVID-19: anti-inflammatory strategies.
- 1.264atıf
- 2020yıl
Kısa özet
COVID-19 enfeksiyonu, TLR ve inflamatuar cisimcik aktivasyonu yoluyla akciğer iltihabına, ateşe ve fibrozise yol açan pro-inflamatuar sitokinler IL-1β ve IL-6'yı tetikler. Yeni sitokinler IL-37 ve IL-38, bu inflamatuar yolları baskılayarak potansiyel terapötik stratejiler sunar.
Yapay zekâ ile başlık ve abstract'tan üretildi; tam metin okunmaz.
Ana noktalar
- COVID-19 enfeksiyonu, TLR ve inflamatuar cisimcik aktivasyonu yoluyla IL-1β ve IL-6 salınımına ve ardından akciğer iltihabına neden olur.
- IL-1β, COVID-19'da akciğer iltihabı, ateş ve fibrozisin anahtar mediyatörüdür.
- IL-37, mTOR ve AMP kinaz yolları aracılığıyla IL-1β, IL-6, TNF ve CCL2'yi inhibe ederek doğal ve edinilmiş bağışıklık yanıtlarını baskılar.
- IL-1 ailesinin yeni bir üyesi olan IL-38 de IL-1β ve diğer pro-inflamatuar sitokinleri baskılayarak terapötik potansiyel sunar.
Yapay zekâ ile başlık ve abstract'tan üretildi; tam metin okunmaz.
Özet (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.
Yazarların özeti; kaynağından alınmıştır. Journal of Biological Regulators and Homeostatic Agents/Journal of Biological Regulators & Homeostatic Agents, 2020 · DOI ↗
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