Differential influences of the BPA, BPS and BPF on in vitro IL-17 secretion by mouse and human T cells

Malaisé, Yann; Mentec, Hélène Le; Sparfel, Lydie; Guzylack‐Piriou, Laurence

doi:10.1016/j.tiv.2020.104993

Cited by 22 publications

(12 citation statements)

References 68 publications

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“…Moreover, BPA has been shown to affect Blimp-1 expression through PPARc (Avila et al 2019), controlling B cell differentiation, which was also reported for TCDD and AHR (Zhang et al 2013). Since BPA can bind to AHR ( Svajger et al 2016;Gao et al 2020;Malais e et al 2020;She and Liu 2020), it is not unlikely that BPA can also control B cell differentiation in an AHR-dependent way. This cooperation between receptors may also explain the contrasting outcomes observed in DC-dependent T cell maturation comparing TCDD and BPA since TCDD act through AHR while BPA can additionally bind to ER and PPAR.…”

Section: Discussionmentioning

confidence: 87%

“…On the other hand, our search found 2 papers supporting the suppression of Treg populations and induction of Th17 cells after BPs exposure in an AHR-dependent manner (Gao et al 2020;Malais e et al 2020). The further search string was widened to include 2 more articles related to NFjB activation by BPA (Dong et al 2020;Wang, Cao, et al 2020).…”

Section: Ahr Mechanistic Pathway In T Cellsmentioning

confidence: 99%

“…A specific mechanism of immunomodulation and immunotoxicity is the activation of AHR by EDCs. (Holsapple et al 1991;Blaylock et al 1992;Malais e et al 2020;Rosenmai et al 2021). AHR activation can lead to both an increase and a decrease of oxidative stress in a ligand-specific manner.…”

Section: Introductionmentioning

confidence: 99%

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EDC-induced mechanisms of immunotoxicity: a systematic review

Vidal

Deepika

Schuhmacher

et al. 2021

Critical Reviews in Toxicology

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Endocrine-disrupting chemicals (EDCs) refer to a group of chemicals that cause adverse effects in human health, impairing hormone production and regulation, resulting in alteration of homeostasis, reproductive, and developmental, and immune system impairments. The immunotoxicity of EDCs involves many mechanisms altering gene expression that depend on the activation of nuclear receptors such as the aryl hydrocarbon receptor (AHR), the estrogen receptor (ER), and the peroxisome proliferator-activated receptor (PPAR), which also results in skin and intestinal disorders, microbiota alterations and inflammatory diseases. This systematic review aims to review different mechanisms of immunotoxicity and immunomodulation of T cells, focusing on T regulatory (Treg) and Th17 subsets, B cells, and dendritic cells (DCs) caused by specific EDCs such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), bisphenols (BPs) and polyfluoroalkyl substances (PFASs). To achieve this objective, a systematic study was conducted searching various databases including PubMed and Scopus to find in-vitro, in-vivo, and biomonitoring studies that examine EDC-dependent mechanisms of immunotoxicity. While doing the systematic review, we found species-and cell-specific outcomes and a translational gap between in-vitro and in-vivo experiments. Finally, an adverse outcome pathway (AOP) framework is proposed, which explains mechanistically toxicity endpoints emerging from different EDCs having similar key events and can help to improve our understanding of EDCs mechanisms of immunotoxicity. In conclusion, this review provides insights into the mechanisms of immunotoxicity mediated by EDCs and will help to improve human health risk assessment.

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Section: Discussionmentioning

confidence: 87%

Section: Ahr Mechanistic Pathway In T Cellsmentioning

confidence: 99%

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EDC-induced mechanisms of immunotoxicity: a systematic review

Vidal

Deepika

Schuhmacher

et al. 2021

Critical Reviews in Toxicology

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“…Yann et al reported that BPF and BPA significantly increased IL-17 production in mouse T cells but not in human T lymphocytes at low and environmentally relevant concentrations. However, BPF, not BPA, could increase IL-17 secretion in mouse naive T cells undergoing Th17 differentiation in vitro ( Malaisé et al, 2020a ). In addition, Yann et al reported that pregnant C3H/HeN mice exposed to 5 or 50 mg/kg body weight of BPA, or BPF daily from gestation day 15 to weaning, exhibited altered immune profiles.…”

Section: Discussionmentioning

confidence: 99%

Transcriptome Changes and Potential Immunotoxicity Analysis in RAW264.7 Macrophages Caused by Bisphenol F

Chen

Zhang

et al. 2022

Front. Pharmacol.

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As a viable substitute for bisphenol A (BPA), BPF has been widely used in the plastic industry and daily consumer goods, resulting in its detection in humans at a comparable concentration. Evidence reveals that BPF and BPA may have similar toxic effects due to their similar structures. However, there is less information about BPF and its latent implications on the immune system, which is associated with many disorders. In this study, the in vitro toxicity of BPF on RAW264.7 macrophages was explored. The cells were treated with different concentrations of BPF (5, 10, 20, 50, 100, and 200 μM), the cell viability and apoptosis were detected, the gene expression profile was analyzed by whole-transcriptome sequencing, and the mRNA levels were detected by qRT-PCR. The results showed a high concentration of BPF could significantly reduce the survival rate of RAW264.7 macrophages. Although the medium concentration (20–50 μM) of BPF seemed to have no impact on the cell activity of macrophages, it caused the occurrence of apoptosis. The results of differential transcription showed that compared with the control group, 121 genes were upregulated and 82 genes were downregulated in the BPF group. The significantly changed gene functions were mainly concentrated in cell cycle, phagosome, lysosome, and antigen processing and presentation. These findings provide valuable information for correctly understanding the immunotoxicity risk of BPF and may help to improve the hazard identification of bisphenol compounds.

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“…Furthermore, exposure to BPs could also promote significant disturbances in the endogenous inflammatory response [ 76 , 77 , 78 , 79 ]. The body’s inflammatory responses play key roles in developing obesity and metabolic disorders [ 80 ].…”

Section: Possible Mechanisms Of Actionmentioning

confidence: 99%

Exposure to Bisphenol A Substitutes, Bisphenol S and Bisphenol F, and Its Association with Developing Obesity and Diabetes Mellitus: A Narrative Review

Alharbi

Algonaiman

Alduwayghiri

et al. 2022

IJERPH

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Bisphenol A, a well-known endocrine-disrupting chemical, has been replaced with its analogs bisphenol S (BPS) and bisphenol F (BPF) over the last decade due to health concerns. BPS and BPF are present in relatively high concentrations in different products, such as food products, personal care products, and sales receipts. Both BPS and BPF have similar structural and chemical properties to BPA; therefore, considerable scientific efforts have investigated the safety of their exposure. In this review, we summarize the findings of relevant epidemiological studies investigating the association between urinary concentrations of BPS and/or BPF with the incidence of obesity or diabetes. The results showed that BPS and BPF were detected in many urinary samples at median concentrations ranging from 0.03 to 0.4 µg·L−1. At this exposure level, BPS median urinary concentrations (0.4 µg·L−1) were associated with the development of obesity. At a lower exposure level (0.1–0.03 µg·L−1), two studies showed an association with developing diabetes. For BPF exposure, only one study showed an association with obesity. However, most of the reported studies only assessed BPS exposure levels. Furthermore, we also summarize the findings of experimental studies in vivo and in vitro regarding our aim; results support the possible obesogenic effects/metabolic disorders mediated by BPS and/or BPF exposure. Unexpectedly, BPS may promote worse obesogenic effects than BPA. In addition, the possible mode of action underlying the obesogenic effects of BPS might be attributed to various pathophysiological mechanisms, including estrogenic or androgenic activities, alterations in the gene expression of critical adipogenesis-related markers, and induction of oxidative stress and an inflammatory state. Furthermore, susceptibility to the adverse effects of BPS may be altered by sex differences according to the results of both epidemiological and experimental studies. However, the possible mode of action underlying these sex differences is still unclear. In conclusion, exposure to BPS or BPF may promote the development of obesity and diabetes. Future approaches are highly needed to assess the safety of BPS and BPF regarding their potential effects in promoting metabolic disturbances. Other studies in different populations and settings are highly suggested.

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Differential influences of the BPA, BPS and BPF on in vitro IL-17 secretion by mouse and human T cells

Cited by 22 publications

References 68 publications

EDC-induced mechanisms of immunotoxicity: a systematic review

EDC-induced mechanisms of immunotoxicity: a systematic review

Transcriptome Changes and Potential Immunotoxicity Analysis in RAW264.7 Macrophages Caused by Bisphenol F

Exposure to Bisphenol A Substitutes, Bisphenol S and Bisphenol F, and Its Association with Developing Obesity and Diabetes Mellitus: A Narrative Review

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