Evidence map›Paper›PMID 30742953›Full record

ReviewBiochimica et biophysica acta. General subjects2019

Mercury-induced inflammation and autoimmunity.

K Michael Pollard, David M Cauvi, Christopher B Toomey, Per Hultman, Dwight H Kono

Open access · greenAbstract readReview
In one paragraph

Review in Biochimica et biophysica acta. General subjects, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed, 1 pooled it
5.5field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

70 citing papers in PubMed, 1 synthesis or guideline pooled it, 139 citations in OpenAlex.

  1. Toxic metal exposure as a possible risk factor for COVID-19 and other respiratory infectious diseases.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2020
    Pooled it
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  18. Membranous Nephropathy after Subcutaneous Mercury Injection.Journal of medical toxicology : official journal of the American College of Medical Toxicology · 2025
    Article
  19. Article
  20. Article

10 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 2 countries.

K Michael PollardDepartment of Molecular Medicine, Scripps Research, 10550 North Torrey Pines Road, La Jolla, CA, 92037, United States of America. Electronic address: mpollard@scripps.edu.
David M CauviDepartment 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. Electronic address: dcauvi@ucsd.edu.
Christopher B ToomeyShiley Eye Institute, Department of Ophthalmology, University of California, San Diego, 9500 Gilman Drive #0946, La Jolla, CA 92093. Electronic address: cbtoomey@ucsd.edu.
Per HultmanDepartment of Experimental and Clinical Medicine, Linköping University, Linköping, Sweden. Electronic address: per.hultman@liu.se.
Dwight H KonoDepartment of Immunology and Microbiology, Scripps Research, 10550 North Torrey Pines Road, La Jolla, CA, 92037, United States of America. Electronic address: dkono@scripps.edu.
Scripps Institution of Oceanography · USUniversity of California, San Diego · USLinköping University · SE

Funding

Medical Scientist Training Program Training GrantT32GM145449 · NIGMS · DUKE UNIVERSITY · PI Christopher D Kontos · 2022 to 2026
$6.6M
Influence of Innate Immunity on Xenobiotic-Induced Systemic AutoimmunityR01ES021464 · NIEHS · SCRIPPS RESEARCH INSTITUTE, THE · PI POLLARD, KENNETH MICHAEL · 2013 to 2017
$3.4M
Xenobiotic-Induced Type 1 Interferon-Independent AutoimmunityR01ES022625 · NIEHS · SCRIPPS RESEARCH INSTITUTE, THE · PI POLLARD, KENNETH MICHAEL · 2014 to 2018
$2.1M
Do Xenobiotics Exacerbate Idiopathic Autoimmunity?R21ES029263 · NIEHS · SCRIPPS RESEARCH INSTITUTE, THE · PI POLLARD, KENNETH MICHAEL · 2018 to 2019
$532k
The effect of age on xenobiotic-induced autoimmunityUH3ES027679 · NIEHS · SCRIPPS RESEARCH INSTITUTE, THE · PI POLLARD, KENNETH MICHAEL · 2018 to 2020
$458k
The effect of age on xenobiotic-induced autoimmunityUH2ES027679 · NIEHS · SCRIPPS RESEARCH INSTITUTE, THE · PI POLLARD, KENNETH MICHAEL · 2016 to 2017
$164k
NIEHS NIH HHS R01 ES021464NIEHS NIH HHS R01 ES022625NIEHS NIH HHS R21 ES029263NIEHS NIH HHS UH2 ES027679NIEHS NIH HHS UH3 ES027679NIGMS NIH HHS T32 GM145449
6 · The paper itself

Abstract

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. 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

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. GENERAL SIGNIFICANCE: Mercury exposure likely contributes to the pathogenesis of autoimmunity.

Indexed as

Autoimmune DiseasesGene Expression RegulationAnimalsAutoimmunityCytokinesDisease Models, AnimalGenome-Wide Association StudyHumansInflammationMercuryCytokinesMercuryAnimal modelAutoimmunityHumanInflammationMercury

Identifiers

PMID30742953
PMCPMC6689266
OpenAlexW2913979495

What Socratic holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.