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Bisphenol AP promotes the development of bleomycin-induced pulmonary fibrosis by regulating macrophage function

ABSTRACT: Bisphenol AP (BPAP), a structural analogue of bisphenol A (BPA), has been frequently detected in humans. The presence of BPAP is linked to various adverse health outcomes, including metabolic diseases and mood disorders. However, the effects by which BPAP contributes to lung diseases remain inadequately understood. This study utilized the mouse macrophage cell line RAW 264.7 and bleomycin induced pulmonary fibrosis model (PF) of C57BL/6 mice to explore the effects of BPAP. Functional experiments demonstrated that BPAP exposure inhibited macrophage proliferation and enhanced oxidative stress. Additionally, BPAP exposure enhanced the phagocytic and chemotactic functions of macrophages.

ORGANISM(S): Mus musculus

PROVIDER: GSE288992 | GEO | 2025/08/21

REPOSITORIES: GEO

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Project description:Bisphenols are used in the process of polymerization of polycarbonate plastics and epoxy resins, which have numerous applications in a variety of consumer products. Due to their hydrophobic properties, bisphenols can easily migrate out of plastic products especially into fatty foods. They have been found in brain, liver, adipose tissue and body fluids, illustrating their environmental prevalence. By increasing colonic inflammation in mice, disrupting the intestinal bacterial community structure and altering the microbial membrane transport system in zebrafish, bisphenols seem to interfere with the gut microbiome. The highly abundant human commensal bacterium Bacteroides thetaiotaomicron was exposed to bisphenols (Bisphenol A (BPA), Bisphenol F (BPF), Bisphenol S (BPS)), to examine the mode of action, in particular of BPF. All chemicals caused a concentration-dependent growth inhibition and the half-maximal effective concentration (EC50) corresponded to their individual logP values, a measure of their hydrophobicity. B. thetaiotaomicron exposed to BPF decreased membrane fluidity with increasing BPF concentrations. Physiological changes including an increase of acetate concentration were observed in cells treated with 0.57 mM BPF. On the proteome level, a higher abundance of several ATP synthase subunits and multidrug efflux pumps suggested an increased energy demand for adaptive mechanisms after BPF exposure. Defence mechanisms were also implicated by a pathway analysis, that identified a higher abundance of members of resistance pathways/strategies to cope with xenobiotics (i.e. antibiotics). Here, we present further insights into the mode of action of bisphenols in a human commensal gut bacterium regarding growth inhibition, and the physiological and functional state of the cell. These results, combined with microbiota-directed effects, could lead to a better understanding of host health disturbances and disease development based on xenobiotic uptake.

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Bisphenol AP promotes the development of bleomycin-induced pulmonary fibrosis by regulating macrophage function

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