The COVID-19 pandemic has brought the world to a standstill, and as scientists and medical professionals continue to race against time to find a cure or vaccine, we are learning more about the virus with every passing day. One of the most devastating consequences of the viral infection is the development of cytokine storms, which can cause severe inflammation and lead to organ failure, and in some cases, even death. However, recent research is shedding light on potential ways to stop cytokine storms in COVID-19, which could prove to be a game-changer in the fight against the pandemic.
New research has uncovered how COVID-19 can cause severe multi-organ damage in patients and possible pathways to prevent cytokine storms, according to a study published in the Journal of Clinical Investigation Insight. The discovery implies a change in how cytokine-storm related illnesses should be approached, according to the senior author of the article, nephrologist and physician-scientist Sumant Chugh. The researchers employed mouse models to mirror the levels of organ injury and inflammation the virus can cause, and managed to reveal ways to lessen vital organ damage. Patients infected with COVID-19 are known to suffer from a severe immune response, which releases too many cytokines into their bloodstreams. This intense response, also known as a cytokine storm, is at the root of the multi-organ damage that starts with the lungs, leading to critical illness and death from SARS-CoV-2. Once the cytokine storm goes beyond the lungs, it extends to other parts of patients’ bodies, such as their hearts, livers and kidneys, causing injuries and acute glomerular injury in some individuals.
The research model was first developed before the pandemic when Chugh and his team were studying why patients with certain types of kidney disease would experience relapses after catching a cold, despite their disease being under control. The researchers discovered a key genetic flaw in these patients and established a way to mimic the cytokine storm caused by a common cold, which they then incorporated into mouse models. The research provides insight into COVID-19 and the common cold, including why severe inflammatory illnesses, such as myocarditis, pericarditis and liver injury, proteinuria and acute kidney injury, occur in some COVID-19 patients. The study also presents the possibilities for treating COVID-19 with specific dual pathways to prevent cytokine storms compared to a single path. The researchers discovered that the strategy of depleting two cytokines was more effective, particularly with tumor necrosis factor alpha.
According to Chugh, the results will inspire new ways of treating respiratory viral illnesses and the complications that the viruses cause, and this approach may lead to developing animal models for long COVID syndrome. The researchers developed a “cocktail” to replicate major components of the cytokine storm caused by the viruses rather than infect the mice with the SARS-CoV-2 or common cold viruses. These cocktails had toxic effects on the glomeruli, the filtering units of the kidneys, when used at low doses, inducing protein leakage in urine. At higher doses, they affected the hearts, livers, and other parts of the kidneys, leading to acute kidney injury and additional health issues. More research is needed to create better ways of targeting cytokine storms and reducing the long-term effects of COVID-19.
In conclusion, the recent breakthrough discoveries in the field of immunology have unveiled powerful paths towards stopping cytokine storms in COVID-19. With the unparalleled collaboration of scientists and medical professionals globally, we are learning more about this deadly virus and finding ways to protect ourselves from the devastating effects of cytokine storms. As research continues, we remain optimistic that we will discover even more effective treatment options and a vaccine that will ultimately conquer this pandemic. Let us all remain vigilant, take common-sense precautions, and continue to support the brave front-liners and researchers who are working tirelessly to save lives and find a cure. Together, we can and will overcome this crisis.
