Harmful Interactions of Non-Essential Heavy Metals with Cells of the Innate Immune System

Theron, Annette J.; Tintinger, Gregory Ronald; Anderson, Ronald

doi:10.4172/2161-0495.s3-005

Cited by 20 publications

(17 citation statements)

References 112 publications

(116 reference statements)

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“…In addition, Hg can accelerate and exacerbate disease manifestations in inbred strains of mice prone to autoimmune disease (Reviewed by Theron et al (2012)). Total mercury levels in livers of porpoises stranded in the southern North Sea varied widely within individuals; adult porpoises displayed significantly higher hepatic Hg concentrations compared to juveniles (p o0.0001).…”

Section: Non Essential Elementsmentioning

confidence: 99%

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Harbour porpoises (Phocoena phocoena) stranded along the southern North Sea: An assessment through metallic contamination

Mahfouz

Henry

Courcot

et al. 2014

Environmental Research

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a b s t r a c tThroughout the last few years, the southern North Sea has witnessed an increase in the number of stranded marine mammals, particularly the harbour porpoise (Phocoena phocoena). This species is subject to several potential threats such as exposure to contaminants, changes in food supply, marine traffic and fishery by-catch. The aims of this study were to investigate potential associations between contaminants and health status and to analyze spatial and temporal trends of metal concentrations in harbour porpoises. Selected trace elements (As, Cd, Cr, Cu, Hg, Mn, Se, V and Zn) were measured in kidneys and livers of 105 harbour porpoises stranded along the southern North Sea (French and Belgian coasts from 2006 to 2013) and 27 stranded along the Bay of Biscay (French coast from 2009 to 2012). Porpoises that died from infectious disease displayed significant higher hepatic concentrations of Cd, Hg, Se and Zn compared to healthy porpoises that died from physical trauma. Adult porpoises displayed significant higher concentrations of Cd, Cr, Hg, Se and V in livers compared to juveniles. No spatial or temporal trends in metal concentrations were detected in our study. The results of the present study suggested that chemical contamination may represent one of many threats encountered by harbour porpoises, but it cannot explain alone the increase in the number of stranded individuals.

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Section: Non Essential Elementsmentioning

confidence: 99%

“…Therefore, this observed correlation between V and Cr may be related to an age-dependant bioaccumulation. Mn and Cr are essential trace elements (Theron et al, 2012) hence slightly variable from animal to animal. Mn is required as a cofactor in at least two classes of enzymes, phosphotransferases and arginases (Mackey et al, 1995).…”

Section: Essential Elementsmentioning

confidence: 99%

Harbour porpoises (Phocoena phocoena) stranded along the southern North Sea: An assessment through metallic contamination

Mahfouz

Henry

Courcot

et al. 2014

Environmental Research

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“…Firstly, the subjects were resident in a major city (Dublin, Republic of Ireland); secondly, most of the heavy metals tested (As, Cd, Hg) are also present in diesel emissions [60]. In addition, residing in areas with high levels of atmospheric pollution has also been reported to be associated with particularly high concentrations of As in nasal mucosa and nasal polyps [59].…”

Section: Outdoor and Indoor Atmospheric Pollution Pulmonary Inflammamentioning

confidence: 99%

“… smoke-mediated, pro-oxidative activation of the transcription factor, nuclear factor kappa B (NFκB), in cells of the airway innate immune system, as well as structural cells, by smoke-derived ROS/radicals and sulphydryl-reactive heavy metals [57][58][59]. On a cautionary note, however, the extent of the involvement of NFκB in the pro-inflammatory effects of smoking has recently been re-visited and questioned, raising the issue of alternative mechanisms of smoke-activated pulmonary inflammation [60].…”

Section: Pro-inflammatory Effects Of Smokingmentioning

confidence: 99%

Smoking and Air Pollution as Pro-Inflammatory Triggers for the Development of Rheumatoid Arthritis

Anderson

Meyer

Ally

et al. 2016

NICTOB

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Smoking is now well recognised not only as a risk factor for rheumatoid arthritis (RA), but also as a determinant of disease activity, severity, response to therapy, and possibly mortality. Recent studies have provided significant insights into the molecular and cellular mechanisms which underpin the pathogenesis of smokingrelated RA. These involve release of the enzymes, peptidylarginine deiminases (PADs) 2 and 4 from smoke-activated, resident and infiltrating pulmonary phagocytes. PADs, in turn, mediate the conversion of various endogenous proteins to putative citrullinated autoantigens. In genetically susceptible individuals, these autoantigens trigger the production of anti-citrullinated peptide/protein pathogenic autoantibodies (ACPA), an event which precedes the development of RA. This review is focused primarily on smoking-mediated harmful chronic inflammatory responses, both local and systemic, which promote the formation of ACPA, as well as the possible involvement of other types of outdoor and indoor pollution in the pathogenesis of RA. This is preceded by a brief overview of the evidence implicating smoking as a risk factor for development of ACPA-positive RA.Keywords: Anti-citrullinated peptide/protein antibodies; airway microbiota; atmospheric pollution; heavy metals; peptidylarginine deiminases; smoking cessation strategies. ImplicationsChronic inflammatory mechanisms operative in the lungs of smokers lead to the production of anti-citrullinated protein antibodies which, in turn, drive the development of rheumatoid arthritis. These mechanistic insights not only reinforce the association between smoking and risk for rheumatoid arthritis, but also the necessity to increase the level of awareness in those at highest risk.

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“…Cadmium mechanisms of toxicity can affect multiple organs and tissues, including the immune function reflected by a broad range of effects in different immune cells. The effects can be different between the vast spectrum of immune cell types, ranging from an increase of some parameters such as phagocytosis of phagocytes, to decrease other functions such as cytokine signalling and secretion of immunoglobulins (Krocova, Macela, Kroca, & Hernychova, 2000;Theron, Tintinger, & Anderson, 2012). However, the extent of the mechanisms of toxicity and the functional effects of cadmium (and other heavy metals) between different immune cell types from small mammal species are not well characterized.…”

Section: Introductionmentioning

confidence: 99%

Cell‐specific immune‐modulation of cadmium on murine macrophages and mast cell lines in vitro

García-Mendoza

Han

Berg

et al. 2019

J of Applied Toxicology

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Toxic trace metals are widespread contaminants that are potentially immunotoxic even at environmentally low exposure levels. They can modulate the immunity to infections, e.g., in wildlife species living in contaminated areas. The diverse immune cell types can be differentially affected by the exposure leading to the modulation of specific protective mechanisms. Macrophages and mast cells, part of the innate immune system, trigger immune responses and perform particular effector functions. The present study compared toxicological and functional effects of cadmium in two models of murine macrophages (RAW264.7 and NR8383 cell lines) and two models of murine mast cells (MC/9 and RBL‐2H3 cell lines). Cadmium was selected as a model compound because its known potential to induce reactive oxygen species and its relevance as an environmental contaminant. Mechanisms of toxicity, such as redox imbalance and apoptosis induction were measured in stationary cells, while functional outcome effects were measured in activated cells. Cadmium‐depleted glutathione antioxidant in all four cell lines tested although reactive oxygen species was not significantly increased. Mast cells had full dose‐response depletion of glutathione below cytotoxic levels while in macrophages the depletion was not complete. Functional endpoints tumour necrosis factor‐alpha and nitrite production in lipopolysaccharide‐activated macrophages were increased by cadmium exposure. In contrast, mast cell lipopolysaccharide‐induced tumour necrosis factor‐alpha and IgE‐mediated histamine release were reduced by cadmium. These data indicate potentially differential effects of cadmium among murine innate immune cell types, where mast cells would be more susceptible to oxidative stress and their function might be at a higher risk to be modulated compared to macrophages.

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Harmful Interactions of Non-Essential Heavy Metals with Cells of the Innate Immune System

Cited by 20 publications

References 112 publications

Harbour porpoises (Phocoena phocoena) stranded along the southern North Sea: An assessment through metallic contamination

Harbour porpoises (Phocoena phocoena) stranded along the southern North Sea: An assessment through metallic contamination

Smoking and Air Pollution as Pro-Inflammatory Triggers for the Development of Rheumatoid Arthritis

Cell‐specific immune‐modulation of cadmium on murine macrophages and mast cell lines in vitro

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