Antibody-based arthritis drug could treat extreme COVID-19
06 September, 2020
A recent study has revealed that an antibody-based blockade might effectively treat cytokine release syndrome (CRS) and alleviate serious cases of COVID-19.
A team of researchers at the Osaka University and Osaka Habikino Medical Center in Japan conducted the recent study. They have now published their findings in the journal Proceedings of the National Academy of Sciences.
The global race to build up a vaccine for SARS-CoV-2 continues. For the time being, researchers are trying to find methods to effectively treat COVID-19, testing both existing drugs and new, experimental therapies.
Because scientists usually do not grasp the mechanisms behind serious COVID-19, many doctors are treating it by following sepsis treatment guidelines.
Could cytokines be the answer?
In this recent study, the scientists centered on cytokines. These are several small proteins that modulate the immune response to trauma, infection, and conditions such as cancer.
Among other things, cytokines activate inflammation, which is the main healing process.
Sometimes, your body releases an excessive amount of cytokines. This causes excess inflammation, that may damage tissues. This response is called a cytokine storm.
Cytokine storms, or CRS, occur in several conditions, including multiple sclerosis, pancreatitis, and COVID-19.
Without treatment, CRS could cause multiple organ failure and, sometimes, death.
The body releases various cytokines during CRS, including interleukin (IL)-2, IL-6, IL-8, IL-10, interferon-gamma, monocyte chemotactic protein-1 (MCP-1), and tumor necrosis factor-alpha. However, there are no specific immunotherapies because of its treatment.
High degrees of several specific cytokines
“Despite knowing which cytokines are involved, there continues to be no specific immunotherapy for CRS, and treatment is bound to supportive care,” says study lead author Sujin Kang.
“To raised understand the molecular mechanisms of CRS pathogenesis,” she adds, “we first studied the cytokine profiles of 91 patients identified as having CRS connected with bacterial sepsis, acute respiratory distress syndrome, or burns.”
The researchers discovered that all three groups of folks had similar cytokine profiles.
Specifically, the researchers measured high degrees of IL-6, IL-8, IL-10, and MCP-1, in addition to a protein called plasminogen activator inhibitor-1 (PAI-1). This protein could cause small blood clots in vessels in the lungs and other organs.
PAI-1 levels drastically higher
Previous studies have displayed that increased PAI-1 levels are linked to more extreme cases of pneumonia, which is a leading reason behind death among persons with COVID-19.
“Study of cytokine profiles in severe COVID-19 patients revealed a rise in IL-6 early in the condition process, triggering release of PAI-1 from arteries,” says senior study author Tadamitsu Kishimoto, a professor at the Osaka University Immunology Frontier Research Center.
“Interestingly, PAI-1 levels were substantially higher in COVID-19 patients with extreme respiratory impediment.”
Higher degrees of IL-6 were associated with higher degrees of the other cytokines and PAI-1. Therefore, the researchers believe that IL-6 signaling could possibly be a significant driver of CRS.
Arthritis drug decreases PAI-1
To research the role of IL-6 in CRS, the researchers gave the participants injections of a human monoclonal antibody-based drug called tocilizumab (Actemra), which blocks IL-6 signaling. The Food and Drug Administration (FDA) have approved tocilizumab as a treatment for rheumatoid arthritis.
The results showed that whenever people with serious COVID-19 received tocilizumab, the degrees of PAI-1 decreased in the blood. Also, the drug alleviated symptoms and improved critical illness in those with severe COVID-19.
Overall, the researchers conclude that IL-6 signaling blockade with the anti-inflammatory medication tocilizumab may reveal new therapeutic opportunities for the treating both CRS and the extreme respiratory problems of COVID-19.
Source: www.medicalnewstoday.com
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