Autoimmunity and Heavy Metals

Bigazzi, Pierluigi E.

doi:10.1177/096120339400300604

Cited by 81 publications

(31 citation statements)

References 27 publications

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“…This is facilitated by the relatively noninvasive sampling and collection of sera and immune cells. Although this approach has been used successfully by toxicologists in the study of other systems [reviewed in (108)(109)(110)(111)(112)], a review of the literature reveals a paucity of studies dealing with neurotoxic exposures and autoimmune responses (113).…”

Section: Neurocytology Immunology and Immunoprivilegementioning

confidence: 99%

Neuroimmunotoxicology: Humoral Assessment of Neurotoxicity and Autoimmune Mechanisms

El-Fawal¹,

Waterman²,

Feo³

et al. 1999

Environmental Health Perspectives

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The interactions between the nervous and immune systems have been recognized in the development of neurodegenerative disease. This can be exploited through detection of the immune response to autoantigens in assessing the neurotoxicity of environmental chemicals. To test this hypothesis, the following questions were addressed. a) Are autoantibodies to nervous system (NS) antigens detected in populations exposed to environmental or occupational chemicals? In sera of male workers exposed to lead or mercury, autoantibodies, primarily IgG, to neuronal cytoskeletal proteins, neurofilaments (NFs), and myelin basic protein (MBP) were prevalent. These findings were confirmed in mice and rats exposed to either metal. b) Do autoantibodies to NS antigens relate to indices of exposure? In humans exposed to either metal, and similarly in exposed rats, titers of lgG against NFs and MBP significantly correlated with blood lead or urinary mercury, the typical indices of exposure. c) Do autoantibodies correlate with sensorimotor deficits? In workers exposed to lead or mercury, a significant correlation was observed between lgG titers and subclinical deficits. Doses of metals used in rat exposures were subclinical, suggesting that autoantibodies may be predictive of neurotoxicity. d) Is the detection indicative of nervous system pathology? In rats exposed to metals, histopathology indicated central nervous system (CNS) and peripheral nervous system (PNS) damage. In addition there was evidence of astrogliosis, which is indicative of neuronal damage in the CNS, and the presence of lgG concentrated along the blood-brain barrier, as indicated by immunostaining for antibodies. e) Are immune responses to NS antigens pathogenic? Immunoglobulin fractions from rat and human sera interfered with neuromuscular function. These studies suggest that the detection of autoantibodies to NS-specific antigens may be used to monitor the development of neurotoxicity to environmental chemicals and that immune mechanisms may be involved in the progression of neurodegeneration.

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Section: Neurocytology Immunology and Immunoprivilegementioning

confidence: 99%

Neuroimmunotoxicology: Humoral Assessment of Neurotoxicity and Autoimmune Mechanisms

El-Fawal¹,

Waterman²,

Feo³

et al. 1999

Environmental Health Perspectives

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“…Although public health concerns about mercury exposures have generally focused on neurodevelopmental toxicity, mercury, particularly inorganic mercury (iHg), has been extensively studied in animal models for its immunotoxic properties, which include both autoimmunity and immunosuppression. The autoimmune effects of iHg in susceptible rodent strains include induction of specific autoantibodies, polyclonal activation of T and B cells, increased serum immunoglobulin G1 (IgG1) and IgE, cytokine dysregulation, and an immune complex glomerulonephritis (Bigazzi 1994;Griem and Gleichmann 1995;Mathieson 1992;Moszczynski 1997;Pollard and Hultman 1997).…”

mentioning

confidence: 99%

Low-dose exposure to inorganic mercury accelerates disease and mortality in acquired murine lupus.

Via

Nguyen

Niculescu

et al. 2003

Environ Health Perspect

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Inorganic mercury (iHg) is known to induce autoimmune disease in susceptible rodent strains. Additionally, in inbred strains of mice prone to autoimmune disease, iHg can accelerate and exacerbate disease manifestations. Despite these well-known links between iHg and autoimmunity in animal models, no association between iHg alone and autoimmune disease in humans has been documented. However, it is possible that low-level iHg exposure can interact with disease triggers to enhance disease expression or susceptibility. To address whether exposure to iHg can alter the course of subsequent acquired autoimmune disease, we used a murine model of acquired autoimmunity, lupus-like chronic graft-versus-host disease (GVHD), in which autoimmunity is induced using normal, nonautoimmune prone donor and F1 recipient mice resistant to Hg-induced autoimmunity. Our results indicate that a 2-week exposure to low-dose iHg (20 or 200 micro g/kg every other day) to donor and host mice ending 1 week before GVHD induction can significantly worsen parameters of disease severity, resulting in premature mortality. iHg pretreatment clearly worsened chronic lupus-like disease, rather than GVHD worsening iHg immunotoxicity. These results are consistent with the hypothesis that low-level, nontoxic iHg preexposure may interact with other risk factors, genetic or acquired, to promote subsequent autoimmune disease development.

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“…Mercury in high doses is a neurotoxin [7]. The experimental studies, mainly in animals, showed that mercury also affects the immune system by inducing lymphoproliferation and autoimmunity [2,4]. The salient features of the mercury-induced autoimmunity are the ANA and antilaminin antibodies [2,4].…”

Section: Resultsmentioning

confidence: 99%

“…These observations prompted us to examine the possibility of a potential relationship between mercury exposure and autoimmune response in autism. We hypothesized that if autism involved such a connection then autistic children should harbor elevated levels of mercuryinduced autoimmune markers, in particular the antinuclear antibodies (ANA) against nucleolar antigens and the antilaminin antibodies against basement-membrane-derived laminin protein [2,4]. We therefore profiled these two autoimmune markers in autistic and normal children.…”

Section: Introductionmentioning

confidence: 99%

Detection of Antinuclear and Antilaminin Antibodies in Autistic Children Who Received Thimerosal-Containing Vaccines

Singh

Rivas

2004

J Biomed Sci

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Autism, a neurodevelopmental disorder, may involve autoimmune pathogenesis. Since mercury is potentially a risk factor for autoimmunity, we conducted a study of mercury-induced antinuclear and antilaminin antibodies in autistic and normal children who had been pre-administered with thimerosal-containing vaccines. Laboratory analysis by different immunoassays showed that the serum level of these two autoimmune markers did not significantly differ between autistic and normal children. This finding suggests that the mercury as in thimerosal-containing vaccines is likely not related to autoimmune phenomenon in autism.

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Autoimmunity and Heavy Metals

Cited by 81 publications

References 27 publications

Neuroimmunotoxicology: Humoral Assessment of Neurotoxicity and Autoimmune Mechanisms

Neuroimmunotoxicology: Humoral Assessment of Neurotoxicity and Autoimmune Mechanisms

Low-dose exposure to inorganic mercury accelerates disease and mortality in acquired murine lupus.

Detection of Antinuclear and Antilaminin Antibodies in Autistic Children Who Received Thimerosal-Containing Vaccines

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