Fluoxetine eases allergic asthma in mice and points at RORγt in Th17 cells
- In an ovalbumin-driven mouse model of allergic asthma, oral fluoxetine at clinically relevant doses reduced airway inflammatory cell infiltration, eosinophilia, IgE and lung macrophage activation.
- In vitro, it dampened activated macrophages without obvious cytotoxicity, and the Th17 population and RORγt-linked signalling were also modulated.
- Public transcriptomic data, target enrichment, docking and molecular dynamics were used to propose how fluoxetine might engage the RORγt axis; this remains a computational hypothesis.
💡 Points Based on the abstract
The interesting angle is the corticosteroid-insensitive, Th17-high patient, not asthma in general. But 'clinically relevant doses' in mice is a loose phrase for a drug with heavy tissue accumulation in rodents, so I'd want measured lung and plasma exposure first. And docking onto RORγt is a hypothesis generator; without a binding or functional assay, I wouldn't call it the mechanism.