How can COVID-19 infection cause or worsen diabetes?

The team found that exposure to SARS-CoV-2 activates immune cells that in turn destroy beta cells, the pancreatic cells that produce insulin.

“There has long been a hypothesis in the field that some viral infections may lead to type 1 diabetes,” said co-author Shuiping Chen, director of the Center for Genomic Health, professor of surgery, and member of the Hartman Institute for Regenerative Medicine at Weill Cornell Medical College. “But we were able to show how this happens in the context of COVID-19 infection.”

“When someone has severe COVID-19, the first priority is obviously to treat the life-threatening symptoms,” said co-author Dr. Robert Schwartz, professor of medicine at Weill Cornell Medical College and a gastroenterologist and hepatologist at NewYork-Presbyterian/Weill Cornell Medical Center. “But in the future, there may be a way to develop clinical treatments that help avoid subsequent damage to organs like the pancreas.”

Since the early days of the COVID-19 pandemic, doctors caring for patients have noticed that the virus affects a number of organ systems, including not only the lungs, but also the heart, liver, colon and pancreas.

In the new study, the researchers started with pancreatic tissue samples from autopsies of people who died from COVID-19. They noticed that the pancreatic islets, the parts of the pancreas that produce insulin to regulate blood sugar, were damaged.

They then used an analysis technique called GeoMx to study the samples in more detail. This revealed the presence of immune cells called macrophages that cause inflammation in the tissue. These macrophages are responsible for killing pathogens, but they sometimes cause collateral damage to healthy tissue.

To learn more about this activity, the team used a model system developed in Chen’s lab that had never been used before: pancreatic islet organoids (mini-organs) that included both the vascular system and immune cells.

“If we want to use organoids to study how disease progresses, it is important to be able to include components of the immune system in these models,” Chen added.

In this case, after the organs were infected with SARS-CoV-2, they found that the macrophages appeared to kill the beta cells through a type of cell death called apoptosis.

The team also used the organs to study how the pancreas responded to infection with another infectious virus: Coxsackie B4, which has been implicated in the development of type 1 diabetes. They found a similar response in macrophages.

“In the future, this organ system will be useful for looking at other viruses as well,” Schwartz said.

Further research into the signaling molecules that activate macrophages has suggested potential interventions to protect beta cells from damage in patients with severe infections. Although it is too early to start testing any treatments, this is something that may be possible in the future.

This work could also help shed light on the underlying causes of long Covid.

The study was published in the journal Cell Stem Cell.

Source: Medical Express