Bisphenol A modulates the metabolic regulator oestrogen-related receptor-α in T-cells

Cipelli, Riccardo; Harries, Lorna W.; Okuda, Kunio; Yoshihara, Shu; Melzer, David; Galloway, Tamara S.

doi:10.1530/rep-13-0423

Cited by 45 publications

(33 citation statements)

References 56 publications

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“…Treatment of human T cell leukemia line, Jurkat, with BPA is reported to increase the expression of ERα (Cipelli et al, 2014). Similarly, BPA exposure in rats increases the expression of ERα in splenic cells derived from females, but not males (Cao et al, 2013).…”

Section: Discussionmentioning

confidence: 99%

Bisphenol A (BPA) stimulates the interferon signaling and activates the inflammasome activity in myeloid cells

Panchanathan

Liu

Leung

et al. 2015

Molecular and Cellular Endocrinology

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Environmental factors contribute to the development of autoimmune diseases, including systemic lupus erythematosus (SLE), which exhibits a strong female bias (female-to-male ratio 9:1). However, the molecular mechanisms remain largely unknown. Because a feedforward loop between the female sex hormone estrogen (E2) and type I interferon (IFN-α/β)-signaling induces the expression of certain p200-family proteins (such as murine p202 and human IFI16) that regulate innate immune responses and modify lupus susceptibility, we investigated whether treatment of myeloid cells with bisphenol A (BPA), an environmental estrogen, could regulate the p200-family proteins and activate innate immune responses. We found that treatment of murine bone marrow-derived cells (BMCs) and human peripheral blood mononuclear cells with BPA induced the expression of ERα and IFN-β, activated the IFN-signaling, and stimulated the expression of the p202 and IFI16 proteins. Further, the treatment increased levels of the NLRP3 inflammasome and stimulated its activity. Accordingly, BPA-treatment of BMCs from non lupus-prone C57BL/6 and the lupus-prone (NZB × NZW)F1 mice activated the type I IFN-signaling, induced the expression of p202, and activated an inflammasome activity. Our study demonstrates that BPA-induced signaling in the murine and human myeloid cells stimulates the type I IFN-signaling that results in an induction of the p202 and IFI16 innate immune sensors for the cytosolic DNA and activates an inflammasome activity. These observations provide novel molecular insights into the role of environmental BPA exposures in potentiating the development of certain autoimmune diseases such as SLE.

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Section: Discussionmentioning

confidence: 99%

Bisphenol A (BPA) stimulates the interferon signaling and activates the inflammasome activity in myeloid cells

Panchanathan

Liu

Leung

et al. 2015

Molecular and Cellular Endocrinology

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“…BPA acts as an agonist for the estrogen receptors, inhibits thyroid hormone mediated transcription by acting as an antagonist (Moriyama et al 2002), altered pancreatic beta cell function (Ropero et al 2008). Adverse human health effects including the onset of obesity and cardiovascular disease (Cipelli et al 2014;Lang et al 2008;Melzer et al 2012) and with numerous reproductive and developmental outcomes (Galloway 2015) were observed in exposure to BPA at levels around 0.2-20 ng/ml (In the general population with measured urinary BPA). Phthalate esters are applied as plasticizers to enhance the flexibility and durability of various materials and also used in manufacturing of PVC polymers and plastisol (Gómez and Gallart-Ayala 2018).…”

Section: ˂Fig 2˃mentioning

confidence: 99%

Occurrence, sources, human health impacts and mitigation of microplastic pollution

Karbalaei

Hanachi

Walker

et al. 2018

Environ Sci Pollut Res

447

168

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The presence and accumulation of plastic and microplastic (MP) debris in the natural environment is of increasing concern and has become the focus of attention for many researchers. Plastic debris is a prolific, long-lived pollutant, that is highly resistant to environmental degradation, readily adheres hydrophobic persistent organic pollutants and is linked to morbidity and mortality in numerous aquatic organisms. The prevalence of MPs within the natural environment are a symptom of continuous and rapid growth in synthetic plastic production and mismanagement of plastic waste. Many terrestrial and marine-based processes, including domestic and industrial drainage, maritime activities agricultural runoff and wastewater treatment plants (WWTPs) effluent, contribute to MP pollution in aquatic environments. MPs have been identified in food consumed by human and in air samples, and exposure to MPs via ingestion or inhalation could lead to adverse human health effects. Regulations in many countries have already been established or will soon be implemented to reduce MPs in aquatic environments. This review focuses on the occurrence, sources, and transport of MPs in terrestrial and aquatic environments to highlight potential human health effects, and applicable regulations to mitigate impacts of MPs. This study also highlights the importance of personality traits and cognitive ability in reducing the entry of MPs into the environment.

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“…ERRs can bind estrogen response elements (EREs) and the ERR-response element (ERRE) resulting in crosstalk between ERs and ERRs [ 17 ]. Additionally, ERRs regulate oxidative metabolism and mitochondrial biogenesis in many cells including T cells and macrophages [ 19 , 20 ]. Of particular importance to the adaptive immune system, ERRα regulates T effector cell function and is needed for T effector cell activation and differentiation [ 21 ].…”

Section: Mechanisms Of Immune Modulation and Disease Exacerbation mentioning

confidence: 99%

Developmental Bisphenol A Exposure Modulates Immune-Related Diseases

Huang

Guo

2016

Toxics

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Bisphenol A (BPA), used in polycarbonate plastics and epoxy resins, has a widespread exposure to humans. BPA is of concern for developmental exposure resulting in immunomodulation and disease development due to its ability to cross the placental barrier and presence in breast milk. BPA can use various mechanisms to modulate the immune system and affect diseases, including agonistic and antagonistic effects on many receptors (e.g., estrogen receptors), epigenetic modifications, acting on cell signaling pathways and, likely, the gut microbiome. Immune cell populations and function from the innate and adaptive immune system are altered by developmental BPA exposure, including decreased T regulatory (Treg) cells and upregulated pro-and anti-inflammatory cytokines and chemokines. Developmental BPA exposure can also contribute to the development of type 2 diabetes mellitus, allergy, asthma and mammary cancer disease by altering immune function. Multiple sclerosis and type 1 diabetes mellitus may also be exacerbated by BPA, although more research is needed. Additionally, BPA analogs, such as bisphenol S (BPS), have been increasing in use, and currently, little is known about their immune effects. Therefore, more studies should be conducted to determine if developmental exposure BPA and its analogs modulate immune responses and lead to immune-related diseases.

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Bisphenol A modulates the metabolic regulator oestrogen-related receptor-α in T-cells

Cited by 45 publications

References 56 publications

Bisphenol A (BPA) stimulates the interferon signaling and activates the inflammasome activity in myeloid cells

Bisphenol A (BPA) stimulates the interferon signaling and activates the inflammasome activity in myeloid cells

Occurrence, sources, human health impacts and mitigation of microplastic pollution

Developmental Bisphenol A Exposure Modulates Immune-Related Diseases

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