Nucleocapsid and Spike Proteins of the Coronavirus SARS-CoV-2 Induce IL6 in Monocytes and Macrophages-Potential Implications for Cytokine Storm Syndrome.
Iwona KarwaciakAnna SałkowskaKaja KaraśJarosław DastychMarcin RatajewskiPublished in: Vaccines (2021)
The pandemic of the new coronavirus SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) has led to the deaths of more than 1.5 million people worldwide. SARS-CoV-2 causes COVID-19, which exhibits wide variation in the course of disease in different people, ranging from asymptomatic and mild courses to very severe courses that can result in respiratory failure and death. Despite the rapid progression of knowledge, we still do not know how individual cells of the immune system interact with the virus or its components, or how immune homeostasis becomes disrupted, leading to the rapid deterioration of a patient's condition. In the present work, we show that SARS-CoV-2 proteins induce the expression and secretion of IL-6 by human monocytes and macrophages, the first line cells of antiviral immune responses. IL-6 may play a negative role in the course of COVID-19 by inhibiting Th1-dependent immunity and stimulating Th17 lymphocytes, thus leading to an increased probability of a cytokine storm.
Keyphrases
- sars cov
- respiratory syndrome coronavirus
- induced apoptosis
- immune response
- respiratory failure
- cell cycle arrest
- coronavirus disease
- peripheral blood
- signaling pathway
- dendritic cells
- endothelial cells
- poor prognosis
- case report
- extracorporeal membrane oxygenation
- endoplasmic reticulum stress
- intensive care unit
- early onset
- cell proliferation
- loop mediated isothermal amplification
- quantum dots
- acute respiratory distress syndrome
- long non coding rna
- pluripotent stem cells
- induced pluripotent stem cells