Effects of 4-Nonylphenol and/or Diisononylphthalate on THP-1 Cells: Impact of Endocrine Disruptors on Human Immune System Parameters

Bennasroune, Amar; Rojas, Leticia; Foucaud, Laurent; Goulaouic, S.; Laval-Gilly, Philippe; Ficková, M; Couleau, Nicolas; Durandet, C.; Henry, Sonia; Falla, Jaı̈ro

doi:10.1177/039463201202500206

Cited by 35 publications

(30 citation statements)

References 31 publications

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“…EDCs have been shown to alter the immune function of macrophages via decreased ERK1/2 phosphorylation . One study revealed that NP activated neutrophils through the activation of protein kinase C, p38 kinase, and ERK .…”

Section: Discussionmentioning

confidence: 99%

Nonylphenol increases tumor formation and growth by suppressing gender‐independent lymphocyte proliferation and macrophage activation

Lee

Han

Park

et al. 2017

Environmental Toxicology

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Nonylphenol (NP) is a well-known endocrine disruptor that influences sexual and reproductive development. Here, we investigated whether NP affects immune responses that are associated with tumor initiation and progression. When spleen cells were incubated with lipopolysaccharide (LPS) and concanavalin A in the presence of 10 M NP, the proliferation of B and T lymphocytes was reduced compared with that in controls, in a gender-independent fashion. While 10 M NP also decreased the production of nitric oxide (NO) in LPS-stimulated bone marrow-derived macrophages (BMDMs), no changes in NO production were detected following treatment with 10 M NP. LPS-stimulated expression of iNOS, COX2, IL-6 and TNF-α in BMDMs was reduced after 6 or 18 hours of incubation with 10 M NP. Furthermore, when mice were pre-exposed to NP for 7 days prior to the injection of B16F10 melanoma cells, the rates of tumor nodule formation and relative tumor growth were higher than those in the control group. In vivo immunosuppressive effect was also clarified by the inhibition of proliferation in B/T lymphocyte and cytokine production in peritoneal macrophages from the mice pretreated with NP for 7 days. Taken together, these data demonstrate that NP could affect the immune responses of lymphocytes and macrophages, leading to the suppression of their tumor-preventing ability. This suggests that individuals at high risk for tumor development should avoid frequent exposure to NP and other endocrine disruptors.

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Section: Discussionmentioning

confidence: 99%

Nonylphenol increases tumor formation and growth by suppressing gender‐independent lymphocyte proliferation and macrophage activation

Lee

Han

Park

et al. 2017

Environmental Toxicology

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“…This is especially very important in our modern world, where hormone-like endocrine disruptors are present in increasing number and increasing amount. There are many data that these materials can alter normal immune functions, phagocytosis included [101][102][103][104][105] and the functional alterations of phagocytosis could cause or promote diseases in the present and future human generations [106][107][108]. …”

Section: Discussionmentioning

confidence: 99%

Is there a hormonal regulation of phagocytosis at unicellular and multicellular levels? A critical review

Csaba

2017

AMicr

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Phagocytosis is an ancient cell function, which is similar at unicellular and multicellular levels. Unicells synthesize, store, and secrete multicellular (mammalian) hormones, which influence their phagocytosis. Amino acid hormones, such as histamine, serotonin, epinephrine, and melatonin stimulate phagocytosis, whereas peptide hormones, such as adrenocorticotropic hormone (ACTH), insulin, opioids, arginine vasopressin, and atrial natriuretic peptide decreased it, independently on their chemical structure or function in multicellulars. Macrophage phagocytosis of multicellulars is also stimulated by amino acid hormones, such as histamine, epinephrine, melatonin, and thyroid hormones, however, the effect of peptide hormones is not uniform: prolactin, insulin, glucagon, somatostatin, and leptin have positive effects, whereas ACTH, human chorionic gonadotropin, opioids, and ghrelin have negative ones. Steroid hormones, such as estrogen, hydrocortisone, and dexamethasone are stimulating macrophage phagocytosis, whereas progesterone, aldosterone, and testosterone are depressing it. Considering the data and observations there is not a specific phagocytosis hormone, or a hormonal regulation of phagocytosis neither unicellular, nor multicellular level, however, hormones having specific functions in multicellulars also influence phagocytosis at both levels universally (in unicellulars) or individually (in macrophages). Nevertheless, the hormonal influence cannot be neglected, as phagocytosis (as a function) is rather sensitive to minute dose of hormones and endocrine disruptors. The hormonal influence of phagocytosis by macrophages can be deduced to the events at unicellular level.

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“…Couleau et al demonstrated that several EDCs reduced phagocytosis of differentiated THP-1 cells, and disturbed TNF-a, Il-1b and IL-8 cytokine secretions, as well as decreased ERK ½ phosphorylation was associated to EDC treatments (Couleau et al, 2015). Moreover, several studies have reported similar results, showing that EDCs directly affect the innate immune system (Bennasroune et al, 2012;Ohnishi et al, 2008;Roy et al, 2012;Watanabe et al, 2003).…”

Section: Comparison Of Cnms Moamentioning

confidence: 90%

Multi-omics analysis of ten carbon nanomaterials effects highlights cell type specific patterns of molecular regulation and adaptation

et al. 2018

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New strategies to characterize the effects of engineered nanomaterials (ENMs) based on omics technologies are emerging. However, given the intricate interplay of multiple regulatory layers, the study of a single molecular species in exposed biological systems might not allow the needed granularity to successfully identify the pathways of toxicity (PoT) and, hence, portraying adverse outcome pathways (AOPs). Moreover, the intrinsic diversity of different cell types composing the exposed organs and tissues in living organisms poses a problem when transferring in vivo experimentation into cell-based in vitro systems.To overcome these limitations, we have profiled genome-wide DNA methylation, mRNA and microRNA expression in three human cell lines representative of relevant cell types of the respiratory system, A549, BEAS-2B and THP-1, exposed to a low dose of ten carbon nanomaterials (CNMs) for 48 h. We applied advanced data integration and modelling techniques in order to build comprehensive regulatory and functional maps of the CNM effects in each cell type.We observed that different cell types respond differently to the same CNM exposure even at concentrations exerting similar phenotypic effects. Furthermore, we linked patterns of genomic and epigenomic regulation to intrinsic properties of CNM. Interestingly, DNA methylation and microRNA expression only partially explain the mechanism of action (MOA) of CNMs. Taken together, our results strongly support the implementation of approaches based on multi-omics screenings on multiple tissues/cell types, along with systems biology-based multi-variate data modelling, in order to build more accurate AOPs.

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Effects of 4-Nonylphenol and/or Diisononylphthalate on THP-1 Cells: Impact of Endocrine Disruptors on Human Immune System Parameters

Cited by 35 publications

References 31 publications

Nonylphenol increases tumor formation and growth by suppressing gender‐independent lymphocyte proliferation and macrophage activation

Nonylphenol increases tumor formation and growth by suppressing gender‐independent lymphocyte proliferation and macrophage activation

Is there a hormonal regulation of phagocytosis at unicellular and multicellular levels? A critical review

Multi-omics analysis of ten carbon nanomaterials effects highlights cell type specific patterns of molecular regulation and adaptation

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