ArticleImmunity, inflammation and disease2026
Propolis Flavonoids Ameliorate Chronic Osteomyelitis in a Rat Model by Modulating TAZ-Regulated Treg/Th17 Balance.
Article in Immunity, inflammation and disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed.
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- Propolis Flavonoids Ameliorate Chronic Osteomyelitis in a Rat Model by Modulating TAZ-Regulated Treg/Th17 Balance.Immunity, inflammation and disease · 2026Article
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4 authors.
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Abstract
objectiveTo investigate the therapeutic mechanism of propolis flavonoids (PF) in chronic osteomyelitis (COM) through transcriptional coactivator with PDZ-binding motif (TAZ)-mediated regulation of regulatory T cell (Treg)/T helper 17 (Th17) cell homeostasis.
methodsSixty 3-month-old Wistar rats were randomly divided into control, model, and PF-treated groups. In vitro, human peripheral blood mononuclear cells (PBMCs) and rat PBMCs were stratified into five treatment groups: control (10% healthy control (HC) serum), osteomyelitis model (15 ng/mL transforming growth factor-β1
resultsPF administration significantly upregulated TAZ protein expression compared to untreated osteomyelitis models (p < 0.05). PF treatment significantly reduced bacterial burden in bone tissue (p < 0.001). In the PF group, Th17 cell proportions increased (2.28 ± 0.35%) compared to the osteomyelitis model group (1.58 ± 0.31%) and RORγt expression was elevated, coupled with reduced Treg populations (1.66 ± 0.27%) compared to the osteomyelitis model group (11.5 ± 0.29%) and reduced FOXP3 levels. Notably, pro-inflammatory cytokines IL-17 and IL-21 decreased in PF-treated groups, while anti-inflammatory IL-10 and IL-2 increased. Periosteal cell proliferation rates improved significantly with PF intervention. TEAD1 overexpression attenuated PF-mediated effects in both human and rat PBMCs, confirming TAZ's central regulatory role across species.
conclusionPropolis flavonoids ameliorate chronic osteomyelitis through TAZ-dependent mechanisms that rebalance Treg/Th17 polarization and promote bacterial clearance. This involves restoring Th17 cell populations while concurrently suppressing their key effector cytokines, ultimately reducing inflammatory pathology and promoting bone repair.
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