MAIT cell activation is reduced by direct and microbiota-mediated exposure to bisphenols
[Display omitted] Oral uptake is the primary route of human bisphenol exposure, resulting in an exposure of the intestinal microbiota and intestine-associated immune cells. Therefore, we compared the impact of bisphenol A (BPA), bisphenol F (BPF) and bisphenol S (BPS) on (i) intestinal microbiota, (...
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| Published in: | Environment international Vol. 158; p. 106985 |
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| Main Authors: | , , , , , , , , |
| Format: | Journal Article |
| Language: | English |
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01-01-2022
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| Abstract | [Display omitted]
Oral uptake is the primary route of human bisphenol exposure, resulting in an exposure of the intestinal microbiota and intestine-associated immune cells. Therefore, we compared the impact of bisphenol A (BPA), bisphenol F (BPF) and bisphenol S (BPS) on (i) intestinal microbiota, (ii) microbiota-mediated immunomodulatory effects and (iii) direct effects on mucosal-associated invariant T (MAIT) cells in vitro. We acutely exposed human fecal microbiota, Bacteroides thetaiotaomicron and Escherichia coli to BPA and its analogues BPF and BPS referring to the European tolerable daily intake (TDI), i.e. 2.3 µg/mL, 28.3 µg/mL and 354.0 µg/mL. Growth and viability of E. coli was most susceptible to BPF, whereas B.thetaiotaomicron and fecal microbiota were affected by BPA > BPF > BPS. At 354.0 µg/mL bisphenols altered microbial diversity in compound-specific manner and modulated microbial metabolism, with BPA already acting on metabolism at 28.3 µg/mL. Microbiota-mediated effects on MAIT cells were observed for the individual bacteria at 354.0 µg/mL only. However, BPA and BPF directly modulated MAIT cell responses at low concentrations, whereby bisphenols at concentrations equivalent for the current TDI had no modulatory effects for microbiota or for MAIT cells. Our findings indicate that acute bisphenol exposure may alter microbial metabolism and impact directly on immune cells. |
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| AbstractList | Oral uptake is the primary route of human bisphenol exposure, resulting in an exposure of the intestinal microbiota and intestine-associated immune cells. Therefore, we compared the impact of bisphenol A (BPA), bisphenol F (BPF) and bisphenol S (BPS) on (i) intestinal microbiota, (ii) microbiota-mediated immunomodulatory effects and (iii) direct effects on mucosal-associated invariant T (MAIT) cells in vitro. We acutely exposed human fecal microbiota, Bacteroides thetaiotaomicron and Escherichia coli to BPA and its analogues BPF and BPS referring to the European tolerable daily intake (TDI), i.e. 2.3 µg/mL, 28.3 µg/mL and 354.0 µg/mL. Growth and viability of E. coli was most susceptible to BPF, whereas B. thetaiotaomicron and fecal microbiota were affected by BPA > BPF > BPS. At 354.0 µg/mL bisphenols altered microbial diversity in compound-specific manner and modulated microbial metabolism, with BPA already acting on metabolism at 28.3 µg/mL. Microbiota-mediated effects on MAIT cells were observed for the individual bacteria at 354.0 µg/mL only. However, BPA and BPF directly modulated MAIT cell responses at low concentrations, whereby bisphenols at concentrations equivalent for the current TDI had no modulatory effects for microbiota or for MAIT cells. Our findings indicate that acute bisphenol exposure may alter microbial metabolism and impact directly on immune cells. [Display omitted] Oral uptake is the primary route of human bisphenol exposure, resulting in an exposure of the intestinal microbiota and intestine-associated immune cells. Therefore, we compared the impact of bisphenol A (BPA), bisphenol F (BPF) and bisphenol S (BPS) on (i) intestinal microbiota, (ii) microbiota-mediated immunomodulatory effects and (iii) direct effects on mucosal-associated invariant T (MAIT) cells in vitro. We acutely exposed human fecal microbiota, Bacteroides thetaiotaomicron and Escherichia coli to BPA and its analogues BPF and BPS referring to the European tolerable daily intake (TDI), i.e. 2.3 µg/mL, 28.3 µg/mL and 354.0 µg/mL. Growth and viability of E. coli was most susceptible to BPF, whereas B.thetaiotaomicron and fecal microbiota were affected by BPA > BPF > BPS. At 354.0 µg/mL bisphenols altered microbial diversity in compound-specific manner and modulated microbial metabolism, with BPA already acting on metabolism at 28.3 µg/mL. Microbiota-mediated effects on MAIT cells were observed for the individual bacteria at 354.0 µg/mL only. However, BPA and BPF directly modulated MAIT cell responses at low concentrations, whereby bisphenols at concentrations equivalent for the current TDI had no modulatory effects for microbiota or for MAIT cells. Our findings indicate that acute bisphenol exposure may alter microbial metabolism and impact directly on immune cells. Oral uptake is the primary route of human bisphenol exposure, resulting in an exposure of the intestinal microbiota and intestine-associated immune cells. Therefore, we compared the impact of bisphenol A (BPA), bisphenol F (BPF) and bisphenol S (BPS) on (i) intestinal microbiota, (ii) microbiota-mediated immunomodulatory effects and (iii) direct effects on mucosal-associated invariant T (MAIT) cells in vitro. We acutely exposed human fecal microbiota, Bacteroides thetaiotaomicron and Escherichia coli to BPA and its analogues BPF and BPS referring to the European tolerable daily intake (TDI), i.e. 2.3 µg/mL, 28.3 µg/mL and 354.0 µg/mL. Growth and viability of E. coli was most susceptible to BPF, whereas B.thetaiotaomicron and fecal microbiota were affected by BPA > BPF > BPS. At 354.0 µg/mL bisphenols altered microbial diversity in compound-specific manner and modulated microbial metabolism, with BPA already acting on metabolism at 28.3 µg/mL. Microbiota-mediated effects on MAIT cells were observed for the individual bacteria at 354.0 µg/mL only. However, BPA and BPF directly modulated MAIT cell responses at low concentrations, whereby bisphenols at concentrations equivalent for the current TDI had no modulatory effects for microbiota or for MAIT cells. Our findings indicate that acute bisphenol exposure may alter microbial metabolism and impact directly on immune cells. |
| ArticleNumber | 106985 |
| Author | Zenclussen, A.C. Chang, H.D. Krause, J.L. Pierzchalski, A. von Bergen, M. Rolle-Kampczyk, U. Herberth, G. Nunes da Rocha, U. Engelmann, B. |
| Author_xml | – sequence: 1 givenname: J.L. surname: Krause fullname: Krause, J.L. organization: Helmholtz-Centre for Environmental Research - UFZ, Department of Environmental Immunology, Leipzig, Germany – sequence: 2 givenname: B. surname: Engelmann fullname: Engelmann, B. organization: Helmholtz-Centre for Environmental Research - UFZ, Department of Molecular Systems Biology, Leipzig, Germany – sequence: 3 givenname: U. surname: Nunes da Rocha fullname: Nunes da Rocha, U. organization: Helmholtz-Centre for Environmental Research - UFZ, Department of Environmental Microbiology, Leipzig, Germany – sequence: 4 givenname: A. surname: Pierzchalski fullname: Pierzchalski, A. organization: Helmholtz-Centre for Environmental Research - UFZ, Department of Environmental Immunology, Leipzig, Germany – sequence: 5 givenname: H.D. surname: Chang fullname: Chang, H.D. organization: present address: German Rheumatism Research Center Berlin, a Leibniz Institute – DRFZ, Schwiete laboratory for microbiota and inflammation, Berlin, Germany – sequence: 6 givenname: A.C. surname: Zenclussen fullname: Zenclussen, A.C. organization: Helmholtz-Centre for Environmental Research - UFZ, Department of Environmental Immunology, Leipzig, Germany – sequence: 7 givenname: M. surname: von Bergen fullname: von Bergen, M. organization: Helmholtz-Centre for Environmental Research - UFZ, Department of Molecular Systems Biology, Leipzig, Germany – sequence: 8 givenname: U. surname: Rolle-Kampczyk fullname: Rolle-Kampczyk, U. organization: Helmholtz-Centre for Environmental Research - UFZ, Department of Molecular Systems Biology, Leipzig, Germany – sequence: 9 givenname: G. surname: Herberth fullname: Herberth, G. email: gunda.herberth@ufz.de organization: Helmholtz-Centre for Environmental Research - UFZ, Department of Environmental Immunology, Leipzig, Germany |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/34991247$$D View this record in MEDLINE/PubMed |
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| Keywords | Batch culture BPS DMSO Immunomodulation MAIT cells EtOH NMDS BPX SCFA PBMC IMDM EU LC-MS/MS BPA Bisphenols TDI In vitro model BPF MAIT Human intestinal microbiota |
| Language | English |
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Oral uptake is the primary route of human bisphenol exposure, resulting in an exposure of the intestinal microbiota and intestine-associated... Oral uptake is the primary route of human bisphenol exposure, resulting in an exposure of the intestinal microbiota and intestine-associated immune cells.... |
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| Title | MAIT cell activation is reduced by direct and microbiota-mediated exposure to bisphenols |
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