Authors
Ivana Ďurišová, Mariana Máčajová, Ingrid Zriniová, Ivana Fábryová, Mailinda Meta, Lenka Bábelová, Boris Bilčík, Aleš Kvasnička, Miroslav Baláž, Soňa Bernátová, Silvia Petrezsélyová, Dominik Filipp, Yuan-Hao Hsu, David Friedecký, Ivan Čavarga, Mária Balážová
Published in
iScience. Volume 29. Issue 9. Pages 117369. Sep 18, 2026. Epub Sep 04, 2026.
Abstract
Pulmonary surfactant lipids support lung homeostasis and innate immunity, and their dysregulation contributes to acute respiratory distress syndrome. Whether mitochondrial phosphatidylglycerol (PG) biosynthesis influences epithelial lipid secretion and inflammatory responses remains unclear. Using A549 cells, we disrupted PGS1, which encodes phosphatidylglycerophosphate synthase, and found that partial loss of PGS1 altered cellular PG levels and changed the secreted phospholipid profile. Valproic acid (VPA), a clinically used antiepileptic drug, similarly remodeled secreted lipids and increased the relative abundance of the anti-inflammatory PG species palmitoyl-oleoyl-phosphatidylglycerol (POPG), an effect not seen with partial PGS1 loss. Functionally, conditioned media from VPA-treated epithelial cells reduced lipopolysaccharide-induced inflammatory responses in PMA-differentiated U937 macrophage-like cells, with lipid extracts contributing to this effect. In a vascularized quail chorioallantoic membrane model, both VPA and POPG decreased inflammation and maintained tissue structure. Overall, these findings connect mitochondrial PG metabolism to epithelial lipid-mediated control of inflammation.
PMID:
42740801
Bibliographic data and abstract were imported from PubMed on 15 Sep 2026.
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