A large number of patients with COVID-19 develop severe and life-threatening hyper-inflammation and acute respiratory distress syndrome (ARDS) and mortality from severe COVID-19 remains high, in part due to the limited range of specific immunomodulatory therapies available.
Patients who survive and those with milder disease, may lose significant tissue function from persistent inflammation and fibrosis, causing chronic lung disease.
Studies have shown the efficacy of dexamethasone in reducing mortality, which indicates the importance of inflammation to disease severity.
New Study Findings
A new study by scientists from the Purdue University and the National Institutes of Health (NIH) demonstrates how an active metabolite of vitamin D, not a form sold over-the-counter, is involved in “switching off” inflammation in the body during infections such as COVID-19.
The researchers analyzed individual lung cells from eight people with COVID-19 and found that in these cells, part of the immune response to SARS-CoV-2 was going into overdrive and exacerbating inflammation in the lungs.
They administered vitamin D in test-tube experiments and observed reduced lung cell inflammation. After which they dove further into how vitamin D achieved this. They did so by turning to T helper cells, also known as CD4+ cells which are a type of immune cell that stimulate the killer T cells and other cells to mount an immune response.
T cells are known to play a role in severe and dangerous cases of COVID-19 by going into overdrive and leading to an often fatal phenomenon known as a cytokine storm.
The scientists found that in normal infections, Th1 cells, which are a subset of helper T cells that fight microbes within the cell, go through a pro-inflammatory phase. During this phase, the body clears the infection.
Shortly after, the system shuts down to move onto the anti-inflammatory phase. The scientists discovered that vitamin D is key in speeding up this transition.
“We found that in healthy T cells, the activation of the inflammatory gene program coincided with the activation of a vitamin D system within these cells. We, therefore, investigated how this vitamin D system works and what it does for healthy T cells before we tried to relate it back to COVID-19,” Dr. Afzali and Dr. Kazemian told the news page, Medical News Today.
Whereas in COVID-19 infections, they saw that the pro-inflammatory phase of Th1 cells did not switch off. They attributed this to either a vitamin D deficiency or an abnormality in the cell’s response to vitamin D.
“Traditionally vitamin D has been thought of as depending on the kidneys to activate it before it becomes functional. We found that T cells had a self-contained system to both fully activate and respond to vitamin D, independently of the kidneys,” they said.
The study suggests that vitamin D could be a therapeutic option for COVID-19 thanks to its role in hyper-inflammation.
“This study reveals a potentially unique role that vitamin D plays in the activation of T-cell functions that regulate inflammation in COVID-19, and understanding these regulatory pathways may provide information that will lead to the development of novel therapies for the treatment of acute COVID-19,” said Dr. Alcendor.
Yasemin Nicola Sakay. (2021, Nov 26). study shows how vitamin D could halt lung inflammation in COVID-19. Medical News Today. Retrieved from:
Chauss, D., Freiwald, T., McGregor, R. et al. Autocrine vitamin D signaling switches off pro-inflammatory programs of TH1 cells. Nat Immunol(2021).