There is growing evidence supporting the anti-inflammatory activity of plant sterols (PS) in preclinical models of intestinal inflammation. However, the underlying mechanisms driving these beneficial effects remain incompletely understood. This study investigates the transcriptional modulatory activity of a PS food supplement (PS-FS) on genes associated with the cellular antioxidant defense system and tight junction (TJ) proteins. A double-chamber coculture model with differentiated Caco-2 cells (apical) and RAW264.7 macrophages (basolateral) was used. Bioaccessible fraction (BF) of PS-FS was obtained following the INFOGEST 2.0 simulated gastrointestinal digestion. A 1/20 dilution of BF was applied to the apical chamber for 90 min, followed by lipopolysaccharide (LPS) stimulation (1 µg/mL, 24 h) on the basolateral side. The interaction between PS-FS and budesonide was also evaluated. The gene expression of Nrf2 (NFE2L2), glutathione S-transferase A1 (GSTA1), NAD(P)H quinone dehydrogenase 1 (NQO1), and heme oxygenase 1 (HMOX-1) was quantified. Additionally, gene expression of TJ-related genes (CLDN1, CLDN3, CLDN4, OCLN, and TJP1) was quantified. Pretreatment with PS-FS significantly increased expression of GSTA1 (26.8%) and HMOX-1 (124.4%) compared to LPS + digestion blank. Furthermore, there was a trend toward increased expression of NFE2L2 and NQO1. Similarly, PS-FS enhanced expression of CLDN3 (33.0%), CLDN4 (211.7%), OCLN (57.1%), and TJP1 (98.9%). However, co-treatment of budesonide and PS-FS resulted in antagonistic interactions. These findings indicate that PS-FS modulates gene expression associated with antioxidant responses and intestinal barrier integrity-related pathways, suggesting to be further developed as a dietary strategy to support the management of inflammatory bowel disease PRACTICAL APPLICATIONS: This research supports the potential use of plant sterol-based food supplements in products aimed at supporting intestinal health. The results suggest that these supplements could help strengthen the gut barrier and support the body's natural antioxidant defenses during intestinal inflammation.

β-Glucan (β-Glu), a bioactive macromolecular polysaccharide known for its immunomodulatory properties, was employed as a nanoparticle carrier to enhance the delivery of budesonide (BUD) in acute bronchial asthma treatment. This study evaluated budesonide- encapsulated β-glucan nanoparticles (BUD@β-Glu NPs) prepared via ionic gelation, which had an average size of 127.6 ± 1.32 nm, a zeta potential of 3.3 ± 0.13 mV, and an 86.7 ± 2.4% encapsulation efficiency. A cumulative release of 72.5% of the drug was achieved after 24 h. In vitro cytocompatibility of BUD@β-Glu NPs was assessed on L929 fibroblast cells using CCK-8 assay. It exhibited remarkable biocompatibility, as indicated by the high cell viability (> 90%) in all groups at 24 h. Using an ovalbumin-induced asthma mouse model, treatment with BUD@β-Glu NPs significantly decreased pro-inflammatory cytokines (IL-4, IL-5, TNF-α) and downregulated p38 MAPK phosphorylation by 65%, indicating effective suppression of airway inflammation. Histological analysis revealed reduced epithelial thickening and mucus production. Notably, BUD@β-Glu NPs increase adherence to nebulizer therapy and reduce airway inflammation in acute bronchial asthma by modulating cytokine signaling. These findings highlight the need for optimized nursing strategies to monitor and enlighten patients on proficient drug delivery systems.