Health
Study reveals how SARS-CoV-2 destroys pancreatic cells and causes diabetes
Using cutting-edge model systems, researchers at Weill Cornell Medicine have uncovered a mechanism by which SARS-CoV-2, the virus that causes COVID-19, induces new cases of diabetes and worsens complications in people who already have it. The team found that exposure to the virus activates immune cells and destroys beta (β) cells, the pancreatic cells that produce insulin. The study was published September 2 in the journal Cell Stem Cell.
“There has long been a hypothesis in the field that certain viral infections can cause type 1 diabetes. However, we have been able to show how this occurs in the context of COVID-19 infection.”
Dr. Chen Shuibin, Co-corresponding author, Director of the Center for Genomic Health, Kiltz Family Professor of Surgery, and member of the Hartman Institute for Therapeutic Organ Regeneration at Weill Cornell Medicine
“For patients with severe COVID-19, the first priority is obviously to treat the life-threatening symptoms,” said co-corresponding author Dr. Robert Schwartz, an associate professor of medicine at Cornell University and a gastroenterologist and hepatologist at NewYork-Presbyterian/Cornell University Medical Center. “But going forward, there may be ways to develop clinical treatments to prevent later damage to organs such as the pancreas.”
Liuliu Yang, PhD, and Yuling Han, PhD, postdoctoral fellows in the Department of Surgery, and Tuo Zhang, PhD, lecturer in microbiology and immunology at Weill Cornell Medicine, are co-first authors of the paper.
From the beginning of the COVID-19 pandemic, doctors treating patients observed that the virus affected many organ systems, including not only the lungs, but also the heart, liver, colon, and pancreas. In this study, researchers took samples of pancreatic tissue from autopsies of people who died from COVID-19. They observed that the islets, the part of the pancreas that produces insulin, which regulates blood sugar levels, were damaged.
The researchers then used an analytical technique called GeoMx to examine the samples in more detail, revealing the presence of immune cells called pro-inflammatory macrophages in the tissue: their role is to kill pathogens, but they can also cause collateral damage to healthy tissue.
To learn more about this activity, the team used a previously unusable model system developed in the Chen lab: pancreatic islet organoids (mini-organs), which contain both vasculature and immune cells. “When using organoids to study disease processes, it's important to be able to include components of the immune system in these models,” said Dr. Chen. In this case, after infecting the organoids with SARS-CoV-2, they found that macrophages appeared to kill beta cells through a type of cell death called pyroptosis.
The team also used the organoids to study how the pancreas responds to infection with another infectious virus, Coxsackievirus B4, which is thought to be involved in the development of type 1 diabetes. They found a similar macrophage response. “In the future, this organoid system may be useful for studying other viruses,” said Dr. Schwartz.
Further research into the signaling molecules that activate macrophages also suggested potential interventions to protect beta cells from damage in patients with severe infection. It is too early to begin testing treatments, but this may be possible in the future. The research may also help elucidate the underlying causes of long COVID, which is thought to affect more than 15 million people in the United States.
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Journal References:
Yang, L. Other(2024). Human vascularized macrophage-islet organoids modeling immune-mediated pancreatic beta cell pyroptosis during viral infection. Cell Stem Cell. doi.org/10.1016/j.stem.2024.08.007.
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