UM studies reveal why diabetics develop severe COVID-19
Ann Arbor – A new study from the University of Michigan recently revealed why people with type 2 diabetes are at increased risk of developing severe cases of COVID-19.
Researchers have identified an enzyme called SETDB2, the same enzyme that can make healing of inflammatory wounds in diabetics difficult, likely to be the cause of severe COVID infections.
After witnessing runaway inflammation in COVID patients at the ICU, researcher W. James Melvin decided to see if there was a possible link between the enzyme and the cases they observed.
Working in Catherine Gallagher’s lab at the Department of Microbiology and Immunology, Michigan Medicine, they started with a mouse model of COVID in diabetic-infected mice and observed a decrease in SETDB2 in immune cells affected by the inflammatory response. ..
Immune cells called macrophages responded similarly in diabetic and severely ill COVID patients. In people, researchers observed the same reaction on monocytes-macrophages based on blood samples.
“I think there’s a reason these patients have cytokine storms,” Melvin said in a statement.
In both human and mouse models, Gallagher and Melvin said lowering SETDB2 increased inflammation. Their study also revealed a pathway that regulates SETDB2, a macrophage known as JAK1 / STAT3, during active COVID infection.
Their results show potential treatment pathways that may benefit in reversing the patterns that diabetic COVID patients tend to exhibit.
The laboratory previously discovered that interferon, an important cytokine of viral immunity, can increase SETDB2 when it responds to wound healing. As part of a new study, researchers found that sera in ICU patients with diabetes and severe COVID infections were more likely to have lower levels of interferon beta compared to non-diabetic patients. ..
“Interferon is being studied throughout the pandemic as a potential treatment, moving back and forth between attempts to raise and lower interferon levels,” Gallagher said in a statement. “In my sense, its effectiveness as a treatment will be unique to both the patient and the timing.”
The researchers were able to reduce inflammatory cytokines and increase SETDB2 in diabetic COVID-infected mice by administering interferon beta.
“We have heard that COVID-19 is increased in IL-1B, TNFalpha, IL-, etc., focusing on those that control SETDB2, one of the many master regulators of these inflammatory cytokines. I’m trying to guess. 6 “Gallerer explained in a statement.
“If you look upstream at what controls SETDB2, interferon is at the top end and JaK1 and STAT3 are in the center. Interferon increases both, which increases SETDB2 in a kind of cascade.”
The importance of identifying a pathway is to present researchers with alternative methods of targeting enzymes, Gallagher said.
“Our study shows that if interferon can target diabetics, especially in the early stages of infection, it can actually make a big difference,” Melvin said in a statement. ..
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