In a groundbreaking study, researchers from Osaka University have unveiled a promising treatment strategy for cytokine storm, a severe inflammatory syndrome triggered by infections or severe burns. Cytokines, crucial chemical messengers in the body, are responsible for eliminating germs and viruses while also managing inflammation. When the immune system overreacts due to a serious infection or burn, it can unleash a cytokine storm, a condition also known as cytokine release syndrome (CRS), which leads to life-threatening inflammation.
One key player in the cytokine storm is Interleukin-6 (IL-6), an essential cytokine that promotes inflammation harmful to the body. During a cytokine storm, IL-6 overproduces, causing a cascade of inflammatory responses. While therapies inhibiting the IL-6 signal have been explored, they often result in long-lasting blockages and adverse effects on the body.
Published in the Proceedings of the National Academy of Sciences (PNAS), the Osaka University researchers introduced a novel strategy to suppress IL-6 signals while minimizing negative treatment effects. They employed an antibody that temporarily inhibits the IL-6 receptor, creating a brief pause in the inflammatory signal. This short-term intervention proved effective in protecting tissues from cytokine storms triggered by conditions like sepsis or severe burns.
Lead author Sujin Kang emphasized the potential of their findings, stating, “Our results suggest that CRS can be treated with an IL-6 receptor antibody that has a short half-life. This can prevent vascular damage and, at the same time, reduce the side effects associated with blocking IL-6.”
Vascular damage, a consequence of infections or burns, occurs when cells lining the inner surface of blood vessels become leaky. The leaked fluid triggers a cytokine storm, potentially causing secondary infections. The researchers also identified a potential mechanism for this damage, revealing that when IL-6 binds to its receptor, it activates a protein called hypoxia-inducible factor-1a (HIF1a), amplifying inflammation.
Senior author Tadamitsu Kishimoto explained the significance of their findings, stating, “We found that blocking the IL-6R-HIF1a signal strengthened vascular endothelial cells and improved vessel integrity. This helped to prevent leakage from the vessels and relieved the inflammation caused by CRS. We hope this will help patients suffering from CRS and other inflammatory diseases in the future.”
This breakthrough could pave the way for more effective treatments for cytokine storms, offering hope for patients facing the life-threatening consequences of severe infections and burns.
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