Nikhil Prasad Fact checked by:Thailand Medical News Team Apr 14, 2025 1 day, 9 hours, 51 minutes ago
Medical News: A groundbreaking international study has uncovered a crucial new link between a specific immune enzyme and the severe lung damage seen in COVID-19 patients suffering from acute respiratory distress syndrome (ARDS). Scientists from the University Hospital Heidelberg in Germany and Harvard Medical School’s Beth Israel Deaconess Medical Center in the United States have discovered that an enzyme known as
adenosine deaminase 2 (ADA2), produced by a type of white blood cell, plays a key role in driving inflammation and scarring in the lungs.
New Study Reveals Enzyme Behind Deadly Lung Inflammation in COVID-19 Patients
ARDS, often fatal, is one of the most severe complications of COVID-19 and is marked by widespread inflammation and fluid build-up in the lungs, making breathing extremely difficult. In this
Medical News report, researchers reveal how ADA2 interacts with a chemical signal called CXCL10 and its receptor CXCR3, which are involved in directing immune cells to areas of infection.
Their findings suggest that ADA2 is not just a bystander, but an active participant in worsening lung injury by encouraging immune cells to release more damaging and scarring substances. This discovery may lead to future treatments that target this enzyme or its related pathways to prevent or reduce the severity of ARDS in viral infections like COVID-19.
Elevated ADA2 Activity Found in Severe COVID-19 Cases
The study analyzed blood and lung tissue samples from COVID-19 patients with and without ARDS. Those suffering from severe ARDS showed significantly elevated levels of ADA2 in their bloodstream. Interestingly, while ADA2 levels in the blood were high, the amount inside the monocytes—the white blood cells producing ADA2—was lower. This suggests that the cells were actively releasing the enzyme into the surrounding environment.
The researchers also found that ADA2 levels in the blood closely matched the levels of CXCL10, a chemical messenger known to attract immune cells that express its receptor, CXCR3. Among ADA2-producing immune cells, the CXCR3 receptor was found to be the most highly expressed compared to other similar receptors, suggesting that these cells are especially drawn to areas of inflammation.
Even more compelling, higher ADA2 activity was linked to lower oxygen levels in the blood, a hallmark of ARDS. This indicates that the more severe the respiratory distress, the higher the ADA2 activity—a potential warning sign of worsening disease.
Monocytes Reprogrammed into Inflammatory and Fibrotic Agents
The team also explored lung tissue using cutting-edge spatial transcriptomics and single-cell RNA sequencing, which allows for highly detailed analysis of gene expression. In lung tissue from COVID-19 patients, ADA2 was most strongly expressed in a type of immune cell called inflammatory CD14high/CD16high monocytes. These cells not only showed high ADA2 levels but also produced genes known to promote inflammation and fibrosis—tiss
ue scarring that makes breathing even more difficult.
In affected lung areas, these cells were found in higher numbers compared to relatively normal lung tissue. This strongly supports the idea that ADA2+ monocytes are not just associated with inflammation, but may be actively remodeling lung tissue in harmful ways.
Possible Pathway to New Treatments
The research paints a picture of a dangerous feedback loop. ADA2, released by monocytes under low-oxygen conditions, may help attract even more damaging immune cells through the CXCL10-CXCR3 axis. These cells then worsen inflammation and scarring in the lungs, further lowering oxygen levels and stimulating more ADA2 release.
The implications are vast. Previous studies have already hinted at ADA2’s involvement in diseases marked by immune overactivity, such as tuberculosis and macrophage activation syndrome. Now, it seems to also play a central role in the lung damage seen in COVID-19.
Blocking ADA2 or disrupting its partnership with the CXCL10-CXCR3 signaling pathway might offer a completely new strategy to prevent or mitigate ARDS in COVID-19 and potentially other infectious diseases that cause similar lung damage.
Conclusions and Future Directions
This study shines a spotlight on the underrecognized but crucial role of ADA2 in COVID-19-induced lung failure. The enzyme’s close relationship with immune signaling pathways and oxygen levels positions it as a potential biomarker for disease severity and a therapeutic target. Although more work is needed—especially since ADA2 is not present in rodent models, making experimental research more challenging—the data opens the door to a deeper understanding of the immune processes that lead to fatal lung inflammation. With further development, therapies that inhibit ADA2 or its related signaling molecules may help save lives in future viral outbreaks and offer relief to patients battling ARDS.
The study findings were published in the peer reviewed International Journal of Molecular Sciences.
https://www.mdpi.com/1422-0067/26/8/3678
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