What is it about?
Acute respiratory distress syndrome, characterized by an aberrant inflammatory response, remains a relatively common and lethal or disabling syndrome. In preclinical models, treatment with the antiviral cytokine interferon-β accelerated the resolution of neutrophil-driven airway inflammation, which could open new avenues for more efficient therapies.
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Why is it important?
Our findings point to a new targeted approach to enhance innate immunity to promote the resolution and repair of lung injury. We show that interferon-β induces complete resolution of neutrophil-driven airway inflammation by countering Toll-like receptor 9-mediated suppression of phagocytosis, neutrophil apoptosis and uptake by macrophages. We also report that the beneficial effects of interferon-β are, in part, mediated by stimulation of the production of specialized pro-resolving lipid mediators, which act through the lipoxin receptor ALX/FPR2. These findings identify an interferon-β-initiated ALX/FPR2-centered resolution program that can be used as a new approach to reduce the severity and mortality associated with acute respiratory distress syndrome.
Perspectives
We provided further support for activation of innate immunity as a viable approach to reprogram inflammatory cells to dampen ongoing inflammatory processes to promote regenerative processes as opposed to the current practice of blocking inflammatory mediators or pathways. Our findings also underscore the therapeutic potential of harnessing the interplay between interferon-β and ALX/FPR2-centered circuits and contribute to advancing “resolution pharmacology” for the treatment of acute respiratory distress syndrome.
Janos Filep
Université de Montréal
Read the Original
This page is a summary of: Interferon-β regulates proresolving lipids to promote the resolution of acute airway inflammation, Proceedings of the National Academy of Sciences, July 2022, Proceedings of the National Academy of Sciences,
DOI: 10.1073/pnas.2201146119.
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