Effect of Bisphenol A on non-specific immunodefenses against non-pathogenic Escherichia coli

Sugita-Konishi, Yoshiko; Shimura, Sumiko; Nishikawa, Tomo; Sunaga, Fujiko; Naito, Hiroyuki; Suzuki, Yoshihiko

doi:10.1016/s0378-4274(02)00388-0

Cited by 65 publications

(53 citation statements)

References 28 publications

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“…In contrast, studies that implied inhibitory effect of BPA on cytokine production had experimental settings that pretreated immune cells with BPA followed by infection (bacteria or virus) or stimulation with lipopolysaccharide. The reduction in cytokine production could be explained by reduced neutrophils activity or downregulation of nitric oxide production caused by BPA exposure, thus leading to inappropriate immune response to defend against invading pathogens (15,22,23). In agreement with the later results, we had shown prenatal BPA exposure to reduce TNF-α response to TLR3 and 4 stimulation, and IL-6 response to TLR7-8 in the neonatal mononuclear cell.…”

Section: Discussionsupporting

confidence: 87%

“…Despite a wide variety of epidemiological and animal studies on the association of BPA with alteration of immune functions and multiple adverse health outcomes (23,26,27), very few researches investigated the effect of BPA exposure on pediatric infectious diseases. While the result from our study did not show prenatal BPA exposure to increase the risk of infection or nasopharyngeal bacterial colonization rate during the first year of life, our finding may contribute to a better understanding of the role of prenatal BPA exposure in childhood infection.…”

Section: Discussionmentioning

confidence: 99%

“…First, the fact that since immune system is composed of multiple cells and variable pathways, suppression of certain cytokines of the innate immune system may not have an overall effect in disease outcome. 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).…”

Section: Discussionmentioning

confidence: 99%

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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: Discussionsupporting

confidence: 87%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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

et al. 2015

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“…90,91) Few reports have appeared concerning BPA and immune function. In vitro, BPA has been shown to inhibit lymphocyte mitogenesis, 92) MCP-1 production, 93) and macrophage adhesion. 94) BPA decreased wet weight of the vagina, decreased volume of the endometrial lamina propria, increased incorporation of bromodeoxyuridine into the DNA of endometrial gland epithelial cells, and increased expression of ERα and progesterone receptor in the luminal epithelium of the endometrium and subepithelial stroma.…”

Section: Bpa and Estrogenic Actionsmentioning

confidence: 99%

Influence of Endocrine-disrupting Chemicals on the Immune System

Nakamura

Kariyazono

2010

JOURNAL OF HEALTH SCIENCE

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Endocrine-disrupting chemicals, i.e., endocrine disruptors (EDs), are exogenous compounds that have the potential to interfere with hormonal regulation and the normal endocrine system and consequently cause side effects on human health. Environmental estrogens, i.e., xenoestrogens, are a diverse group of chemicals that bind to estrogen receptors, mimic estrogenic actions, and may have side effects on human health. Bisphenol A (BPA), which is produced by the acid-catalyzed reaction of acetone and phenol and is widely used in the manufacture of polycarbonate plastics and epoxy resins, is classified into xenoestrogens. Food allergy is caused by individual intolerance towards commonly tolerated foods, and this event derived from an immunological mechanism. Allergic diseases such as urticaria, asthma and anaphylaxis, are known to be connected with the production of specific immunoglobulin (Ig)E to allergens of environmental sources. In this paper, we discuss the relationship of EDs between xenoestrogenic reaction and immune responses in human and animals.

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“…Diethylstilbestrol (DES), a typical oestrogen-like chemical, has been shown in mice to induce immune suppression and reduce elimination of bacteria (L. Monocytogenes) (Pung et al, 1984) and parasites (T. spiralis) (Luebke et al, 1994), possibly because of reduced mobilisation of phagocytising macrophages (Pung et al, 1984). Similarly, the endocrine disrupter bisphenol A, a constituent of certain plastic packaging materials for food, reduced the elimination of E. coli in experimentally infected mice (Sugita-Konishi et al, 2003b).…”

Section: Effects Of Xenobiotics On Host Resistancementioning

confidence: 99%

Interactions between Infections, Nutrients and Xenobiotics

2005

TemaNord

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Effect of Bisphenol A on non-specific immunodefenses against non-pathogenic Escherichia coli

Cited by 65 publications

References 28 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

Influence of Endocrine-disrupting Chemicals on the Immune System

Interactions between Infections, Nutrients and Xenobiotics

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