Chemico-biological interactions · 2026
Exploring potential association between bisphenol A exposure and spondyloarthritis: Integrative evidence from molecular analyses and NHANES.
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Tang Jun, Mo Shiyan, Chen Wenji, Fan Lina, Xiao Rui, Liu Xiaofei
Аннотация
BACKGROUND: Spondyloarthritis (SpA), including ankylosing spondylitis (AS) and psoriatic arthritis (PsA), involves complex interactions between genetic susceptibility and environmental factors. Bisphenol A (BPA), an endocrine-disrupting chemical with immunomodulatory properties, may influence immune regulation, but its relationship with SpA remains unclear.
METHODS: BPA-associated targets (CTD and ChEMBL) and AS- and PsA-related genes (GeneCards and OMIM) were collected. Shared targets were identified through network analysis and hub screening. GEO datasets were used to evaluate shared targets' expression patterns. Molecular docking and 100-ns molecular dynamics simulations assessed BPA interactions with core shared targets. NHANES data were analyzed to evaluate population-level associations between urinary BPA and PsA, as AS assessment was limited by insufficient BPA measurements.
RESULTS: BPA shared 1,076 targets with AS and 598 targets with PsA. Five cytokines (TNF-α, IL-10, IL-6, IL-1β, and IFN-γ) were identified as shared targets. TNF-α was decreased in both AS and PsA datasets, whereas IL-10 was increased in AS and showed an upward trend in PsA. The cytokine signature showed preliminary classification potential in transcriptomic datasets of AS (AUC = 0.831) and PsA (AUC = 0.899), although validation in larger cohorts is required. Molecular simulations supported stable BPA interactions, particularly with TNF-α and IL-10. NHANES analysis showed higher urinary BPA concentrations in PsA participants than controls (1.468 vs. 1.054 ng/mL, P = 0.338).
CONCLUSION: These findings suggest that BPA exposure may be associated with SpA-related immune dysregulation through cytokine networks, particularly the TNF-α/IL-10 axis. However, given the non-significant population-level association, further experimental and longitudinal studies are warranted.
METHODS: BPA-associated targets (CTD and ChEMBL) and AS- and PsA-related genes (GeneCards and OMIM) were collected. Shared targets were identified through network analysis and hub screening. GEO datasets were used to evaluate shared targets' expression patterns. Molecular docking and 100-ns molecular dynamics simulations assessed BPA interactions with core shared targets. NHANES data were analyzed to evaluate population-level associations between urinary BPA and PsA, as AS assessment was limited by insufficient BPA measurements.
RESULTS: BPA shared 1,076 targets with AS and 598 targets with PsA. Five cytokines (TNF-α, IL-10, IL-6, IL-1β, and IFN-γ) were identified as shared targets. TNF-α was decreased in both AS and PsA datasets, whereas IL-10 was increased in AS and showed an upward trend in PsA. The cytokine signature showed preliminary classification potential in transcriptomic datasets of AS (AUC = 0.831) and PsA (AUC = 0.899), although validation in larger cohorts is required. Molecular simulations supported stable BPA interactions, particularly with TNF-α and IL-10. NHANES analysis showed higher urinary BPA concentrations in PsA participants than controls (1.468 vs. 1.054 ng/mL, P = 0.338).
CONCLUSION: These findings suggest that BPA exposure may be associated with SpA-related immune dysregulation through cytokine networks, particularly the TNF-α/IL-10 axis. However, given the non-significant population-level association, further experimental and longitudinal studies are warranted.