Researchers from the University of Hong Kong investigated why people with type 2 diabetes are more likely to experience respiratory complications after COVID-19 and what can be done to prevent this. They discovered that inflammatory immune cells may contribute to lung scarring after a SARS-CoV-2 infection and that GLP-1 medications may offer protection. According to the Centers for Disease Control and Prevention (CDC), about 1 in 8 people in the U.S. has diabetes, and type 2 diabetes makes up more than 90% of cases. Doctors prescribe GLP-1 receptor agonists, including semaglutide and tirzepatide , to treat type 2 diabetes and obesity. Besides improving blood sugar control and promoting weight loss, these drugs may also reduce the risk of cardiovascular and kidney disease. People with type 2 diabetes have a higher risk of developing long COVID and pulmonary fibrosis, a condition where scar tissue builds up in the lungs and makes breathing more difficult.
Researchers from the University of Hong Kong investigated why people with type 2 diabetes are more likely to experience respiratory complications after COVID-19 and what can be done to prevent this.
They discovered that inflammatory immune cells may contribute to lung scarring after a SARS-CoV-2 infection and that GLP-1 medications may offer protection.
According to the Centers for Disease Control and Prevention (CDC), about 1 in 8 people in the U.S. has diabetes, and type 2 diabetes makes up more than 90% of cases.
Doctors prescribe GLP-1 receptor agonists, including semaglutide and tirzepatide , to treat type 2 diabetes and obesity. Besides improving blood sugar control and promoting weight loss, these drugs may also reduce the risk of cardiovascular and kidney disease.
People with type 2 diabetes have a higher risk of developing long COVID and pulmonary fibrosis, a condition where scar tissue builds up in the lungs and makes breathing more difficult.
In the new study, researchers combined analyses of human samples with experiments in mice to better understand how type 2 diabetes contributes to long COVID-related pulmonary fibrosis .
They first analyzed data from an earlier long COVID study involving 90 people hospitalized with COVID-19, including 11 with type 2 diabetes and 79 without. They compared immune cell activity during hospitalization and again 2 to 3 months later, looking for differences in genes linked to inflammation and lung scarring.
Next, they infected diabetic and non-diabetic mice with SARS-CoV-2 to compare the effects of diabetes on long-term lung damage.
In another experiment, the researchers depleted macrophages , immune cells involved in inflammation, to determine whether they contributed to lung scarring after infection.
Finally, they treated infected diabetic mice with a GLP-1 receptor agonist and compared them with untreated mice.
In both the human and mouse experiments, the researchers found consistent evidence linking type 2 diabetes to long COVID-related lung scarring.
In the human analysis, people with type 2 diabetes showed increased activity in monocytes , immune cells that can develop into macrophages, for up to 3 months after COVID-19.
They also had higher levels of genes and proteins linked to inflammation and pulmonary fibrosis than people without diabetes.
The first mouse experiment produced similar results. Diabetic mice developed more severe infections, experienced greater weight loss and higher viral loads, and showed increased activity of a fibrosis-related gene not observed in non-diabetic mice.
In another experiment, diabetic mice had more lung-infiltrating macrophages after SARS-CoV-2 infection than non-diabetic mice.
When researchers removed these immune cells, the mice developed less lung inflammation and scarring, suggesting macrophages play an important role in lung damage.
In the final experiment, the researchers tested whether GLP-1 medications could reduce lung damage. Compared with untreated diabetic mice, treated mice developed significantly less lung scarring.
Additional tests indicated that the drugs altered macrophage responses to infection.