Mercury-induced inflammation and autoimmunity
Human exposure to mercury leads to a variety of pathologies involving numerous organ systems including the immune system. A paucity of epidemiological studies and suitable diagnostic criteria, however, has hampered collection of sufficient data to support a causative role for mercury in autoimmune d...
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| Published in | Biochimica et biophysica acta. General subjects Vol. 1863; no. 12; p. 129299 |
|---|---|
| Main Authors | , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Netherlands
Elsevier B.V
01.12.2019
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| Subjects | |
| Online Access | Get full text |
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| Abstract | Human exposure to mercury leads to a variety of pathologies involving numerous organ systems including the immune system. A paucity of epidemiological studies and suitable diagnostic criteria, however, has hampered collection of sufficient data to support a causative role for mercury in autoimmune diseases. Nevertheless, there is evidence that mercury exposure in humans is linked to markers of inflammation and autoimmunity. This is supported by experimental animal model studies, which convincingly demonstrate the biological plausibility of mercury as a factor in the pathogenesis of autoimmune disease.
In this review, we focus on ability of mercury to elicit inflammatory and autoimmune responses in both humans and experimental animal models.
Although subtle differences exist, the inflammatory and autoimmune responses elicited by mercury exposure in humans and experimental animal models show many similarities. Proinflammatory cytokine expression, lymphoproliferation, autoantibody production, and nephropathy are common outcomes. Animal studies have revealed significant strain dependent differences in inflammation and autoimmunity suggesting genetic regulation. This has been confirmed by the requirement for individual genes as well as genome wide association studies. Importantly, many of the genes required for mercury-induced inflammation and autoimmunity are also required for idiopathic systemic autoimmunity. A notable difference is that mercury-induced autoimmunity does not require type I IFN. This observation suggests that mercury-induced autoimmunity may arise by both common and specific pathways, thereby raising the possibility of devising criteria for environmentally associated autoimmunity.
Mercury exposure likely contributes to the pathogenesis of autoimmunity.
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•Mercury exposure is linked with inflammation, autoantibodies, and renal pathology.•Animal studies recapitulate the immune features of human exposure.•Differences in inflammation and autoimmunity are genetically regulated.•Required genes include those regulating innate and/or adaptive immunity.•Unlike idiopathic autoimmunity type I IFN is not required. |
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| AbstractList | Human exposure to mercury leads to a variety of pathologies involving numerous organ systems including the immune system. A paucity of epidemiological studies and suitable diagnostic criteria, however, has hampered collection of sufficient data to support a causative role for mercury in autoimmune diseases. Nevertheless, there is evidence that mercury exposure in humans is linked to markers of inflammation and autoimmunity. This is supported by experimental animal model studies, which convincingly demonstrate the biological plausibility of mercury as a factor in the pathogenesis of autoimmune disease.
In this review, we focus on ability of mercury to elicit inflammatory and autoimmune responses in both humans and experimental animal models.
Although subtle differences exist, the inflammatory and autoimmune responses elicited by mercury exposure in humans and experimental animal models show many similarities. Proinflammatory cytokine expression, lymphoproliferation, autoantibody production, and nephropathy are common outcomes. Animal studies have revealed significant strain dependent differences in inflammation and autoimmunity suggesting genetic regulation. This has been confirmed by the requirement for individual genes as well as genome wide association studies. Importantly, many of the genes required for mercury-induced inflammation and autoimmunity are also required for idiopathic systemic autoimmunity. A notable difference is that mercury-induced autoimmunity does not require type I IFN. This observation suggests that mercury-induced autoimmunity may arise by both common and specific pathways, thereby raising the possibility of devising criteria for environmentally associated autoimmunity.
Mercury exposure likely contributes to the pathogenesis of autoimmunity.
[Display omitted]
•Mercury exposure is linked with inflammation, autoantibodies, and renal pathology.•Animal studies recapitulate the immune features of human exposure.•Differences in inflammation and autoimmunity are genetically regulated.•Required genes include those regulating innate and/or adaptive immunity.•Unlike idiopathic autoimmunity type I IFN is not required. Human exposure to mercury leads to a variety of pathologies involving numerous organ systems including the immune system. A paucity of epidemiological studies and suitable diagnostic criteria, however, has hampered collection of sufficient data to support a causative role for mercury in autoimmune diseases. Nevertheless, there is evidence that mercury exposure in humans is linked to markers of inflammation and autoimmunity. This is supported by experimental animal model studies, which convincingly demonstrate the biological plausibility of mercury as a factor in the pathogenesis of autoimmune disease.In this review, we focus on ability of mercury to elicit inflammatory and autoimmune responses in both humans and experimental animal models.Although subtle differences exist, the inflammatory and autoimmune responses elicited by mercury exposure in humans and experimental animal models show many similarities. Proinflammatory cytokine expression, lymphoproliferation, autoantibody production, and nephropathy are common outcomes. Animal studies have revealed significant strain dependent differences in inflammation and autoimmunity suggesting genetic regulation. This has been confirmed by the requirement for individual genes as well as genome wide association studies. Importantly, many of the genes required for mercury-induced inflammation and autoimmunity are also required for idiopathic systemic autoimmunity. A notable difference is that mercury-induced autoimmunity does not require type I IFN. This observation suggests that mercury-induced autoimmunity may arise by both common and specific pathways, thereby raising the possibility of devising criteria for environmentally associated autoimmunity.Mercury exposure likely contributes to the pathogenesis of autoimmunity. Background: Human exposure to mercury leads to a variety of pathologies involving numerous organ systems including the immune system. A paucity of epidemiological studies and suitable diagnostic criteria, however, has hampered collection of sufficient data to support a causative role for mercury in autoimmune diseases. Nevertheless, there is evidence that mercury exposure in humans is linked to markers of inflammation and autoimmunity. This is supported by experimental animal model studies, which convincingly demonstrate the biological plausibility of mercury as a factor in the pathogenesis of autoimmune disease. Scope of the review: In this review, we focus on ability of mercury to elicit inflammatory and autoimmune responses in both humans and experimental animal models. Major conclusions: Although subtle differences exist, the inflammatory and autoimmune responses elicited by mercury exposure in humans and experimental animal models show many similarities. Proinflammatory cytokine expression, lymphoproliferation, autoantibody production, and nephropathy are common outcomes. Animal studies have revealed significant strain dependent differences in inflammation and autoimmunity suggesting genetic regulation. This has been confirmed by the requirement for individual genes as well as genome wide association studies. Importantly, many of the genes required for mercury-induced inflammation and autoimmunity are also required for idiopathic systemic autoimmunity. A notable difference is that mercury-induced autoimmunity does not require type I IFN. This observation suggests that mercury-induced autoimmunity may arise by both common and specific pathways, thereby raising the possibility of devising criteria for environmentally associated autoimmunity. General significance: Mercury exposure likely contributes to the pathogenesis of autoimmunity. Human exposure to mercury leads to a variety of pathologies involving numerous organ systems including the immune system. A paucity of epidemiological studies and suitable diagnostic criteria, however, has hampered collection of sufficient data to support a causative role for mercury in autoimmune diseases. Nevertheless, there is evidence that mercury exposure in humans is linked to markers of inflammation and autoimmunity. This is supported by experimental animal model studies, which convincingly demonstrate the biological plausibility of mercury as a factor in the pathogenesis of autoimmune disease. In this review, we focus on ability of mercury to elicit inflammatory and autoimmune responses in both humans and experimental animal models. Although subtle differences exist, the inflammatory and autoimmune responses elicited by mercury exposure in humans and experimental animal models show many similarities. Proinflammatory cytokine expression, lymphoproliferation, autoantibody production, and nephropathy are common outcomes. Animal studies have revealed significant strain dependent differences in inflammation and autoimmunity suggesting genetic regulation. This has been confirmed by the requirement for individual genes as well as genome wide association studies. Importantly, many of the genes required for mercury-induced inflammation and autoimmunity are also required for idiopathic systemic autoimmunity. A notable difference is that mercury-induced autoimmunity does not require type I IFN. This observation suggests that mercury-induced autoimmunity may arise by both common and specific pathways, thereby raising the possibility of devising criteria for environmentally associated autoimmunity. Mercury exposure likely contributes to the pathogenesis of autoimmunity. Human exposure to mercury leads to a variety of pathologies involving numerous organ systems including the immune system. A paucity of epidemiological studies and suitable diagnostic criteria, however, has hampered collection of sufficient data to support a causative role for mercury in autoimmune diseases. Nevertheless, there is evidence that mercury exposure in humans is linked to markers of inflammation and autoimmunity. This is supported by experimental animal model studies, which convincingly demonstrate the biological plausibility of mercury as a factor in the pathogenesis of autoimmune disease.BACKGROUNDHuman exposure to mercury leads to a variety of pathologies involving numerous organ systems including the immune system. A paucity of epidemiological studies and suitable diagnostic criteria, however, has hampered collection of sufficient data to support a causative role for mercury in autoimmune diseases. Nevertheless, there is evidence that mercury exposure in humans is linked to markers of inflammation and autoimmunity. This is supported by experimental animal model studies, which convincingly demonstrate the biological plausibility of mercury as a factor in the pathogenesis of autoimmune disease.In this review, we focus on ability of mercury to elicit inflammatory and autoimmune responses in both humans and experimental animal models.SCOPE OF THE REVIEWIn this review, we focus on ability of mercury to elicit inflammatory and autoimmune responses in both humans and experimental animal models.Although subtle differences exist, the inflammatory and autoimmune responses elicited by mercury exposure in humans and experimental animal models show many similarities. Proinflammatory cytokine expression, lymphoproliferation, autoantibody production, and nephropathy are common outcomes. Animal studies have revealed significant strain dependent differences in inflammation and autoimmunity suggesting genetic regulation. This has been confirmed by the requirement for individual genes as well as genome wide association studies. Importantly, many of the genes required for mercury-induced inflammation and autoimmunity are also required for idiopathic systemic autoimmunity. A notable difference is that mercury-induced autoimmunity does not require type I IFN. This observation suggests that mercury-induced autoimmunity may arise by both common and specific pathways, thereby raising the possibility of devising criteria for environmentally associated autoimmunity.MAJOR CONCLUSIONSAlthough subtle differences exist, the inflammatory and autoimmune responses elicited by mercury exposure in humans and experimental animal models show many similarities. Proinflammatory cytokine expression, lymphoproliferation, autoantibody production, and nephropathy are common outcomes. Animal studies have revealed significant strain dependent differences in inflammation and autoimmunity suggesting genetic regulation. This has been confirmed by the requirement for individual genes as well as genome wide association studies. Importantly, many of the genes required for mercury-induced inflammation and autoimmunity are also required for idiopathic systemic autoimmunity. A notable difference is that mercury-induced autoimmunity does not require type I IFN. This observation suggests that mercury-induced autoimmunity may arise by both common and specific pathways, thereby raising the possibility of devising criteria for environmentally associated autoimmunity.Mercury exposure likely contributes to the pathogenesis of autoimmunity.GENERAL SIGNIFICANCEMercury exposure likely contributes to the pathogenesis of autoimmunity. |
| ArticleNumber | 129299 |
| Author | Cauvi, David M. Hultman, Per Toomey, Christopher B. Kono, Dwight H. Pollard, K. Michael |
| AuthorAffiliation | c Shiley Eye Institute, Department of Ophthalmology, University of California, San Diego, 9500 Gilman Drive #0946, La Jolla, California 92093 a Department of Molecular Medicine, Scripps Research, 10550 North Torrey Pines Road, La Jolla California, 92037 d Department of Experimental and Clinical Medicine, Linköping University, Patologihuset, ing 69, plan 10, Campus US, Linköping, Sweden e Department of Immunology and Microbiology, Scripps Research, 10550 North Torrey Pines Road, La Jolla California, 92037 b Department of Surgery and Center for Investigations of Health and Education Disparities, School of Medicine, University of California, San Diego, 9500 Gilman Drive #0739, La Jolla, California 92093 |
| AuthorAffiliation_xml | – name: a Department of Molecular Medicine, Scripps Research, 10550 North Torrey Pines Road, La Jolla California, 92037 – name: d Department of Experimental and Clinical Medicine, Linköping University, Patologihuset, ing 69, plan 10, Campus US, Linköping, Sweden – name: b Department of Surgery and Center for Investigations of Health and Education Disparities, School of Medicine, University of California, San Diego, 9500 Gilman Drive #0739, La Jolla, California 92093 – name: e Department of Immunology and Microbiology, Scripps Research, 10550 North Torrey Pines Road, La Jolla California, 92037 – name: c Shiley Eye Institute, Department of Ophthalmology, University of California, San Diego, 9500 Gilman Drive #0946, La Jolla, California 92093 |
| Author_xml | – sequence: 1 givenname: K. Michael surname: Pollard fullname: Pollard, K. Michael email: mpollard@scripps.edu organization: Department of Molecular Medicine, Scripps Research, 10550 North Torrey Pines Road, La Jolla, CA, 92037, United States of America – sequence: 2 givenname: David M. surname: Cauvi fullname: Cauvi, David M. email: dcauvi@ucsd.edu organization: Department of Surgery and Center for Investigations of Health and Education Disparities, School of Medicine, University of California, San Diego, 9500 Gilman Drive #0739, La Jolla, CA 92093, United States of America – sequence: 3 givenname: Christopher B. surname: Toomey fullname: Toomey, Christopher B. email: cbtoomey@ucsd.edu organization: Shiley Eye Institute, Department of Ophthalmology, University of California, San Diego, 9500 Gilman Drive #0946, La Jolla, CA 92093 – sequence: 4 givenname: Per surname: Hultman fullname: Hultman, Per email: per.hultman@liu.se organization: Department of Experimental and Clinical Medicine, Linköping University, Linköping, Sweden – sequence: 5 givenname: Dwight H. surname: Kono fullname: Kono, Dwight H. email: dkono@scripps.edu organization: Department of Immunology and Microbiology, Scripps Research, 10550 North Torrey Pines Road, La Jolla, CA, 92037, United States of America |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/30742953$$D View this record in MEDLINE/PubMed https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-162307$$DView record from Swedish Publication Index |
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| Copyright | 2019 Elsevier B.V. Copyright © 2019 Elsevier B.V. All rights reserved. |
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| Keywords | Autoimmunity Animal model HMR1 UNC93B1 mHgIA PHA MHC TNF IFN NLRP CTLA4 TLR ICOS SLC15A4 Human CD IL Con A 4-1BB Inflammation AP3B1 PBMC NFKB1 BCR LAG TACI DAF1 IRF Mercury |
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| Snippet | Human exposure to mercury leads to a variety of pathologies involving numerous organ systems including the immune system. A paucity of epidemiological studies... Background: Human exposure to mercury leads to a variety of pathologies involving numerous organ systems including the immune system. A paucity of... |
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| SubjectTerms | Animal model animal models Animals antibody formation autoimmune diseases Autoimmune Diseases - chemically induced Autoimmune Diseases - genetics Autoimmune Diseases - pathology Autoimmunity Autoimmunity - drug effects cytokines Cytokines - genetics Cytokines - immunology Disease Models, Animal Gene Expression Regulation - drug effects Gene Expression Regulation - immunology genes Genome-Wide Association Study Human Humans immune system Inflammation Inflammation - chemically induced Inflammation - immunology Inflammation - pathology kidney diseases Mercury Mercury - toxicity pathogenesis |
| Title | Mercury-induced inflammation and autoimmunity |
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