Orally Administered Bisphenol A Disturbed Antigen Specific Immunoresponses in the Naïve Condition

Goto, Masao; Takano-Ishikawa, Yuko; Ono, Hiroshi; Yoshida, Mitsuru; Yamaki, Kohji; Shinmoto, Hiroshi

doi:10.1271/bbb.70004

Cited by 52 publications

(37 citation statements)

References 39 publications

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“…Second, several reports have shown cytokine production to respond to BPA in a dose-dependent manner (15,20,21,23). In some studies in which lower doses of BPA were used, no effect was seen on ex vivo immune cell function or disease progression in vivo (22,28,29). Thus, it is possible that the extent of cytokine suppression exposed to low and environmentally relevant BPA level, such as in our study, was not sufficient to significantly increase the risk of infection or nasopharyngeal bacterial colonization in infants.…”

Section: Discussionmentioning

confidence: 99%

Prenatal exposure to bisphenol-A is associated with Toll-like receptor–induced cytokine suppression in neonates

et al. 2015

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Background: Despite widespread human exposure to biphenol A (BPA), limited studies exist on the association of BPA with adverse health outcomes in young children. This study aims to investigate the effect of prenatal exposure to BPA on toll-like receptor-induced cytokine responses in neonates and its association with infectious diseases later in life. Methods: Cord bloods were collected from 275 full-term neonates. Production of TNF-α, IL-6, and IL-10 were evaluated after stimulating mononuclear cells with toll-like receptor ligands (TLR1-4 and 7-8). Serum BPA concentrations were analyzed by enzyme-linked immunosorbent assay. Bacteria from nasopharyngeal specimens were identified with multiplex PCR and culture method. result: Result showed significant association between cord BPA concentration and TLR3-and TLR4-stimulated TNF-α response (P = 0.001) and that of TLR78-stimulated IL-6 response (P = 0.03). Clinical analysis did not show prenatal BPA exposure to be correlated with infection or bacterial colonization during the first year of life. conclusion: This is the first cohort study that indicated prenatal BPA exposure to play a part in TLR-related innate immune response of neonatal infants. However, despite an altered immune homeostasis, result did not show such exposure to be associated with increased risk of infection during early infancy.

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Section: Discussionmentioning

confidence: 99%

Prenatal exposure to bisphenol-A is associated with Toll-like receptor–induced cytokine suppression in neonates

et al. 2015

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“…Genomic DNA was digested and removed using an RNase-Free DNase Kit (Qiagen). First strand cDNA was synthesized using oligo (dT) [12][13][14][15][16][17][18] primer (Invitrogen, Carlsbad, CA, USA) and the Omniscript RT Kit (Qiagen). The synthesized cDNA was thermocycled for PCR amplification with 1 mM each primer and 1.5 U of Taq polymerase.…”

Section: Generation Of Immature Dcs and Their Induction Of Maturationmentioning

confidence: 99%

“…[14][15][16] BPA was reported to enhance IL-4 production by T helper (Th) 2 cells in vitro while also enhancing the Th2 and Th1 immune responses, depending on the doses of BPA administered in vivo. 17,18 These experimental studies have indicated that BPA may help trigger allergic responses.…”

Section: Introductionmentioning

confidence: 99%

Bisphenol A in combination with TNF-α selectively induces Th2 cell-promoting dendritic cells in vitro with an estrogen-like activity

Guo¹,

Liu

Uemura

et al. 2010

Cell Mol Immunol

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Bisphenol A (BPA) is a monomer used in manufacturing a wide range of chemical products, including epoxy resins and polycarbonate. BPA, an important endocrine disrupting chemical that exerts estrogen-like activities, is detectable at nanomolar levels in human serum worldwide. The pregnancy associated doses of 17b-estradiol (E2) plus tumor-necrosis factor-a (TNF-a) induce distorted maturation of human dendritic cells (DCs) that result in an increased capacity to induce T helper (Th) 2 responses. The current study demonstrated that the presence of BPA during DC maturation influences the function of human DCs, thereby polarizing the subsequent Th response. In the presence of TNF-a, BPA treatment enhanced the expression of CC chemokine ligand 1 (CCL1) in DCs. In addition, DCs exposed to BPA/TNF-a produced higher levels of IL-10 relative to those of IL-12p70 on CD40 ligation, and preferentially induced Th2 deviation. BPA exerts the same effect with E2 at the same dose (0.01-0.1 mM) with regard to DC-mediated Th2 polarization. These findings imply that DCs exposed to BPA will provide one of the initial signals driving the development and perpetuation of Th2-dominated immune response in allergic reactions.

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“…Goto et al (2007) studied antigen-specific responses of immune cells after oral administration of BPA (1.5 to 1.8 mg/kg b.w./day) to T cell receptor transgenic mice. BPA induced complex effects on the immune response mainly suppressing antigen-specific cytokine production of T cells.…”

Section: Effects On Signal Transfer and Gene Expressionmentioning

confidence: 99%

Scientific Opinion on Bisphenol A: evaluation of a study investigating its neurodevelopmental toxicity, review of recent scientific literature on its toxicity and advice on the Danish risk assessment of Bisphenol A

Flavourings¹

2010

EFSA Journal

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Bisphenol A (BPA) is used in the manufacture of plastics, to produce reusable drinking bottles, infant feeding bottles and other food storage containers. EFSA was asked to evaluate a dietary developmental neurotoxicity study in rats (Stump, 2009) and recent scientific literature (2007)(2008)(2009)(2010) in terms of relevance for the risk assessment of BPA. The impact of these studies on the current Tolerable Daily Intake (TDI) of 0.05 mg BPA/kg body weight (b.w.)/day as set by EFSA in 2006 was assessed. Advice on the Danish risk assessment underlying the Danish ban of BPA in food contact materials for infants aged 0-3 years is included. Overall, based on this comprehensive evaluation of recent toxicity data, the Panel on food contact materials, enzymes, flavourings and processing aids (CEF) concluded that no new study could be identified, which would call for a revision of the current TDI. This TDI is based on the No-Observed-Adverse-Effect-Level (NOAEL) of 5 mg/kg b.w./day from a multi-generation reproductive toxicity study in rats, and the application of an uncertainty factor of 100. This factor is regarded as conservative based on all information on BPA toxicokinetics. The Panel noted that some studies conducted on developing animals have suggested other BPA-related effects of possible toxicological relevance, in particular biochemical changes in brain, immune-modulatory effects and enhanced susceptibility to breast tumours. These studies had several shortcomings. At present the relevance of these findings for human health cannot be assessed. Should any new relevant data become available in the future, the Panel will reconsider this opinion. A minority opinion is expressed by a Panel member and presented in an Annex to this opinion. © European Food Safety Authority, 2010 KEY WORDSBisphenol A, BPA, CAS No. 00080-05-7, developmental toxicity, neurobehaviour, low dose effects. In order to provide a global view on the risk assessment of Bisphenol A, the CEF Panel decided to address the three mandates as given above in a single opinion and postponed the adoption of this comprehensive document to 23 rd September 2010.The three different questions raised by the Commission are dealt with in three different parts (PARTS I to III) of the opinion. PART IV presents an overview of the conclusions from PARTS I to III, together with an overall conclusion. PART IThe GLP compliant study by Stump (2009) was performed according to OECD guideline 426 to address any uncertainty regarding potential neurodevelopmental effects of BPA. BPA was administered daily in the diet at concentrations of 0, 0.15, 1.5, 75, 750, and 2250 mg/kg feed to female Sprague-Dawley rats from gestational day (GD) 0 to postnatal day (PND) 21. The relative estimated intakes (in mg/kg b.w./day) were 0, 0.01, 0.12, 5.85, 56.4 and 164 during gestation and 0, 0.03, 0.25, 13.1, 129 and 410 during lactation. The CEF Panel considers this treatment schedule as relevant to human exposure in utero and via either breastfeeding or infant bottle feeding (in this...

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Orally Administered Bisphenol A Disturbed Antigen Specific Immunoresponses in the Naïve Condition

Cited by 52 publications

References 39 publications

Prenatal exposure to bisphenol-A is associated with Toll-like receptor–induced cytokine suppression in neonates

Prenatal exposure to bisphenol-A is associated with Toll-like receptor–induced cytokine suppression in neonates

Bisphenol A in combination with TNF-α selectively induces Th2 cell-promoting dendritic cells in vitro with an estrogen-like activity

Scientific Opinion on Bisphenol A: evaluation of a study investigating its neurodevelopmental toxicity, review of recent scientific literature on its toxicity and advice on the Danish risk assessment of Bisphenol A

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