Inorganic arsenic impairs proliferation and cytokine expression in human primary T lymphocytes

Morzadec, Claudie; Bouezzedine, Fidaa; Macoch, Mélinda; Fardel, Olivier; Vernhet, Laurent

doi:10.1016/j.tox.2012.05.025

Cited by 57 publications

(44 citation statements)

References 37 publications

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“…We did not find interaction effect of the two metals on T helper memory cells. However, common modes of action of the two metals are possible, as both metals have been reported to target the thymus, to demonstrate suppressed T cell function, and involve inflammation and NRF2 pathways [8, 23–26]. A decrease in Th memory cells in humans has been shown to increase susceptibility to infections [27].…”

Section: Discussionmentioning

confidence: 99%

Cord blood T cell subpopulations and associations with maternal cadmium and arsenic exposures

Nygaard

Palys

et al. 2017

PLoS ONE

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BackgroundArsenic and cadmium are environmental pollutants, and although the evidence for adverse immune effects after prenatal arsenic and cadmium exposures is increasing, little is known about the underlying immunological mechanisms.MethodsWe investigated the relationship between prenatal arsenic and cadmium exposures and a variety of T cell subpopulations measured in cord blood for 63 participants in the New Hampshire Birth Cohort Study. Post-partum toenail concentrations of arsenic and cadmium were used as an estimate of maternal exposure during pregnancy. The characteristics of cord blood proportions of T lymphocytes and subpopulations (expression of markers for Th1, Th2, Th17, Th1Th17, induced and natural regulatory T cells and NKTs) are presented.ResultsIn regression analyses, maternal arsenic exposure levels were inversely associated with cord blood T helper memory cells (-21%, 95% CI: -36%, -3%) and the association was found to be stronger in females. They were also inversely associated with activated T helper memory cells, particularly in males (-26%, 95% CI: -43%, -3%). Similarly, inverse associations were observed between cadmium exposure levels and activated T helper memory cells (-16%, 95% CI: -30%, -1%) and also for T helper memory cells in females (-20%, 95% CI: -35%, -3%).ConclusionThe results suggest that prenatal exposures to relatively low levels of arsenic and cadmium may contribute to altered distribution of T cell populations at birth. These changes in theory, could have contributed to the previously reported immunosuppressive effects observed later in infancy/childhood.

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Section: Discussionmentioning

confidence: 99%

Cord blood T cell subpopulations and associations with maternal cadmium and arsenic exposures

Nygaard

Palys

et al. 2017

PLoS ONE

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“…A biphasic dose-dependent response was observed following As III or As V exposure of mitogen-stimulated human and bovine PBMC [119], demonstrating As immunosuppressive effects depend on the dose. As markedly suppressed lymphocyte secretion and/or mRNA levels of IFN-γ, IL-4 and IL-10 in different in vitro models [114,116,117]. As III also significantly impaired differentiation of human Th17 cells by repressing their expression and release of IL-17 and decreasing expression of RORγt, which regulates IL-17, through inactivation of JNK/c-Jun pathway [120].…”

Section: In Vitro Studiesmentioning

confidence: 99%

Arsenic immunotoxicity: a review

2013

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Exposure to arsenic (As) is a global public health problem because of its association with various cancers and numerous other pathological effects, and millions of people worldwide are exposed to As on a regular basis. Increasing lines of evidence indicate that As may adversely affect the immune system, but its specific effects on immune function are poorly understood. Therefore, we conducted a literature search of non-cancer immune-related effects associated with As exposure and summarized the known immunotoxicological effects of As in humans, animals and in vitro models. Overall, the data show that chronic exposure to As has the potential to impair vital immune responses which could lead to increased risk of infections and chronic diseases, including various cancers. Although animal and in vitro models provide some insight into potential mechanisms of the As-related immunotoxicity observed in human populations, further investigation, particularly in humans, is needed to better understand the relationship between As exposure and the development of disease.

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“…In normal reactions, T-cells (and their functional sub-populations), B-cells, and mononuclear phagocytes all are key to the tuberculin reactions. Notably, there are time-related shifts in T-cell subtypes during the course of this response (Konttinen et al 1983;Morzadec et al 2012), with variations in the local proportion/numbers of CD4 þ and CD8 þ cells playing an active role in the generation of any positive tuberculin reaction. Intra-dermal administration of avian tuberculin here would be expected to stimulate T-cells with minimal effects on B-cells and result in increased cytokine/chemokine release and recruitment of an array of immune cells (mostly macrophages, neutrophils, etc.…”

Section: Discussionmentioning

confidence: 99%

Immunosuppressive effects of arsenic in broiler chicks exposed to Newcastle disease virus

Sattar

Khan

Hussain

et al. 2016

Journal of Immunotoxicology

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To assess the effects of prolonged exposure to arsenic (As, as arsenate) on host immune competence overall and resistance to Newcastle disease (ND) viral infection in particular, a study was carried out in broiler chicks. At 7 days of age, chicks were assigned to groups that would undergo varying vaccination, challenge, and/or As exposures; Group 1 was a control; Group 2 was to receive Newcastle disease virus (NDV) only; two groups (Groups 3, 4) were to be given As daily (50 mg/kg, by gavage) from Days 7-35 of the experiment. All groups underwent normal vaccination on Days 5, 23, and 32 against live NDV (B1 type, LaSota strain); two groups (Groups 2, 4) were challenged with field-isolated NDV at Day 24. At Days 14, 21, 28, and 35 of age, subsets of chicks in each group were evaluated. The results showed feed intake and weight gain were lower in As-treated and NDV-challenged chicks. In As-treated chicks, absolute and relative spleen weights were significantly greater, whereas those of the thymus significantly lower, over the entire 35-day period. Effects on bursa weights (absolute, relative) were only significantly reduced through Day 21. Antibody titers against ND were significantly reduced (vs. control) over the whole 35 days in birds that received As alone, but only significantly depressed through the first 21 days in birds that received As þ NDV; thereafter, titers were significantly greater (in parallel with effects in birds that received NDV alone). In contrast, antibody responses to T-dependent antigen (Sheep red blood cells [SRBC]) were significantly lower in As only-and As þ NDV-treated chicks throughout the study period. Among birds exposed to As (alone or with NDV), in situ phagocytic activity was elevated and cutaneous sensitivity responses decreased during the period from Day 28 to Day 35. NDV alone had spurious effects on phagocytic activity but did cause significant reductions in cutaneous sensitivity responses. It was concluded that arsenic decreased immunity in broiler chicks, thereby making them prone to ND. ARTICLE HISTORY

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Inorganic arsenic impairs proliferation and cytokine expression in human primary T lymphocytes

Cited by 57 publications

References 37 publications

Cord blood T cell subpopulations and associations with maternal cadmium and arsenic exposures

Cord blood T cell subpopulations and associations with maternal cadmium and arsenic exposures

Arsenic immunotoxicity: a review

Immunosuppressive effects of arsenic in broiler chicks exposed to Newcastle disease virus

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