"Thimerosol is the preservative in immunisation shots, so anytime you get an immunisation shot you are undergoing the same procedure that in the University Lab that we used to give animals auto-immune disease---give a little tiny injection of mercury. And when you get an immunisation shot you are getting a little tiny dose of mercury there."---Hal Huggins DDS
Bernaudin JF, Druet E, Druet P, Masse R.Inhalation or ingestion of organic or inorganic mercurials produces auto-immune disease in rats.Clin Immunol Immunopathol. 1981 Jul;20(1):129-35. No abstract available.PMID: 7021027 [PubMed - indexed for MEDLINE]
The linkage between xenobiotic exposures and autoimmune diseases remains to be clearly defined. However, recent studies have raised the possibility that both genetic and environmental factors act synergistically at several stages or checkpoints to influence disease pathogenesis in susceptible populations. These observations predict that individuals susceptible to spontaneous autoimmunity should be more susceptible following xenobiotic exposure by virtue of the presence of predisposing background genes. To test this possibility, mouse strains with differing genetic susceptibility to murine lupus were examined for acceleration of autoimmune features characteristic of spontaneous systemic autoimmune disease following exposure to the immunostimulatory metals nickel and mercury. Although NiCl(subscript)2(/subscript) exposure did not exacerbate autoimmunity, HgCl(subscript)2(/subscript) significantly accelerated systemic disease in a strain-dependent manner. Mercury-exposed (NZB X NZW)F(subscript)1(/subscript) mice had accelerated lymphoid hyperplasia, hypergammaglobulinemia, autoantibodies, and immune complex deposits. Mercury also exacerbated immunopathologic manifestations in MRL+/+ and MR (italic)-lpr (/italic)mice. However, there was less disease acceleration in (italic)lpr(/italic) mice compared with MRL+/+ mice, likely due to the fact that environmental factors are less critical for disease induction when there is strong genetic susceptibility. Non-major histocompatability complex genes also contributed to mercury-exacerbated disease, as the nonautoimmune AKR mice, which are H-2 identical with the MRL, showed less immunopathology than either the MRL/(italic)lp(/italic)r or MRL+/+ strains. This study demonstrates that genetic susceptibility to spontaneous systemic autoimmunity can be a predisposing factor for HgCl(subscript)2(/subscript)-induced exacerbation of autoimmunity. Such genetic predisposition may have to be considered when assessing the immunotoxicity of xenobiotics. Additional comparative studies using autoimmune-prone and nonautoimmune mice strains with different genetic backgrounds will help determine the contribution that xenobiotic exposure makes in rendering sensitive populations susceptible to autoimmune diseases.
Human exposure to certain compounds or therapeutic drugs can result in the development of an autoimmune syndrome. Mercury (Hg) induced autoimmunity is one of the few animal models in which administration of a chemical induces a specific loss of tolerance to self-antigens. After receiving subtoxic doses of Hg or other heavy metals, susceptible mouse strains rapidly develop highly specific antibodies to nucleolar antigens. In addition, these animals display a general activation of the immune system, especially pronounced for the Th2 subset and a transient glomerulonephritis with immunoglobulin deposits. Like many human autoimmune diseases, this syndrome is associated with the expression of susceptible major histocompatibility complex (MHC) class II genes. In this article, we review the essential features of this model, and we discuss the putative mechanisms by which Hg creates such a severe immune dysfunction.