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A dynamic duo of cells identified in lung blood vessels: Scientists identify subtypes of lung endothelial cells that promote inflammation, regeneration

Scientists at the University of Illinois Chicago have analyzed gene expression data from more than 35,000 blood vessel cells from the lungs of mice and identified two subtypes.

One subtype, which they call immune endothelial cells, or immuneECs, preferentially expressed more genes involved in inflammation and the regulation of the immune response. The devEC subtype, for developmental endothelial cells, expressed more genes involved in cell development, like cell regeneration and proliferation.

The findings are published in the journal JCI Insight. They could lead to better treatments for lung infections, which can be dangerously exacerbated by unchecked inflammation.

The UIC team, led by Dr. Jalees Rehman, classified the subtypes by extracting lung tissue from mice engineered to express a fluorescent protein only in the blood vessel endothelial cells. Using a fluorescence cell sorter, the scientists isolated the lung endothelial cells. They then sequenced RNA from thousands of individual endothelial cells and categorized them based on their prominent gene signatures.

They found multiple groups of endothelial cells, with two dominant cell types — immuneECs and devECs — which changed over time during inflammation.

“Across our experiments, consistently we observed that the blood vessel cells of the lung seem to have these different functions and groupings, and the two predominant groups become even more distinct when responding to infection or stress,” said Rehman, UIC professor in the department of pharmacology and regenerative medicine and the department of medicine at the College of Medicine. “Importantly, we also analyzed publicly available datasets of human lungs and found similar distinct groups of endothelial cells as we had observed in the mouse lungs.”

In their experiments, Rehman and his colleagues studied cells from mice with healthy lungs and mice with lungs that were injured or fighting infections due to a bacterial toxin or influenza virus. While both subtypes were present in healthy and sick lungs, the gene expression profiles of each subtype further diverged in response to infections or injury.

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