Researchers at Philipps-Universität Marburg have uncovered why the chronic lung disease COPD often worsens acutely during influenza infections: the signaling molecule CXCL11 is produced in increased amounts in response to the viral infection and disrupts the balance of the airways. As a result, not only is excessive, thick mucus produced, but the natural antiviral defense is also weakened. These mechanisms could serve as targeted therapeutic entry points in the future.
The research group led by DZL investigators Prof. Dr. Mareike Lehmann and Prof. Dr. Bernd Schmeck reports these findings in the current issue of the journal Thorax.
For their investigations, the team used human-based model systems derived from airway epithelial cells that closely mimic key structural and functional properties of the respiratory epithelium. These models were experimentally infected with influenza viruses and subsequently characterized using high-resolution single-cell analyses. This approach enabled the precise identification of cell type–specific changes and molecular signaling pathways mediated by CXCL11.
“Such studies are only possible in Marburg because of the close integration of clinical care and molecular basic research. This allows us to transfer questions arising directly from patient care into experimental models – and to translate the insights gained back into the clinical setting,” says Prof. Dr. Mareike Lehmann of Philipps-Universität Marburg.
The findings provide an important starting point for preventing or more effectively treating acute COPD exacerbations in the future. In the long term, therapeutic strategies targeting CXCL11 could help reduce mucus overproduction and strengthen the antiviral defense of the airways.
Further Information: Institut für Lungenforschung
Original publication: Melo-Narvaez et al, Single-cell mapping reveals CXCL11 as a driver of mucus production and inflammation in influenza A virus exacerbation in COPD, Thorax (2026) https://doi.org/10.1136/thorax-2025-224202
