Sulforaphane has been investigated in human pathologies and preclinical models of airway diseases. To provide further mechanistic insights, we explored L-sulforaphane (LSF) in the ovalbumin (OVA)-induced chronic allergic airways murine model, with key hallmarks of asthma. Histological analysis indicated that LSF prevented or reversed OVA-induced epithelial thickening, collagen deposition, goblet cell metaplasia, and inflammation. Well-known antioxidant and anti-inflammatory mechanisms contribute to the beneficial effects of LSF.Fourier transform infrared microspectroscopy revealed altered composition of macromolecules, including lipids, following OVA-sensitization, which were restored by LSF. RNA sequencing in human peripheral blood mononuclear cells highlighted the anti-inflammatory signature of LSF.Novel findings indicated that LSF reduced the expression and activity of histone deacetylase 8.Further, LSF resulted in histone and -tubulin hyperacetylation in vivo. More generally, this study identified new epigenetic regulatory mechanisms accounting for the protective effects and provide support for the potential clinical utility of LSF in allergic airways disease.

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