Re: TH-17 response is the key.

Here are studies on Mercury and how it affects the immune system. I dont think the key is to concentrate on the microbiology of it. How it affects T-cells or B cells, etc. because frankly, we are all different. But mercury, is a wrench in the gears. It's water in the engine. It's sand in the gun. It is a thing that binds to anything and everything and destroys your body on a surreptitious level because it is a small ELEMENT. Basically it f***s up your nerves (video evidence shows neurons and dendrites shriveling up in the presence of mercury. Due to the fact that mercury immobilizes the building process of the nerve), your immune system, your kidneys, pretty much all your cells. They are presented with lots of lipid peroxidation (destruction of the cell's phospholipid bilayer membranes causing lysing and damage) and oxidative stress.


here are some studies:

"Polymorphonuclear phagocytosis and killing in workers exposed to inorganic mercury"; Int. J. Immunopharmacol; 12:16:1011-7; 1994; Dec; Perlingeiro RC; Queroz ML.

"The ability of nuetrophils to phagocytose and kill Candida species as well as the splenic phagocytic function were investigated in workers from a mercury-producing plant. In the nuetrophil phagocytosis study, two species of Candida were used since in individuals with myleperoxidase deficiency nuetrophils are unable to kill Candida albicans, while Candida psuedotropicalis can be effectively lysed. Phagocytosis of both antigens and splenic phagocytic function were normal in all the workers studied. However, following ingestion of the organisms there was considerable reduction in the ability of nuetrophils from exposed workers to kill both species of Candida, and this was not explained by a mild impairment of phagocytosis. After improvement in the hygiene conditions in the factory, a new evaluation was performed, 6 months later, in the same workers and urinary mercury concentrations were determined monthly in each worker. Despite a significant reduction in urinary mercury concentrations, a greater impairment in the ability of neutrophils to kill C. albicans was observed. The killing of C. psuedotropicallis presented no further impairment when compared to the previous evaluation. These results suggest that impairment of the lytic activity of the nuetrophils from workers with urinary mercury concentrations within the safe level for exposed population is due, at least in part, to some interference with myeloperoxidase activity. In addition, the mercury-NADPH complex, once formed, could limit the reduced pyridine nucleotides by NADPH-dependent enzymes such as NADPH oxidase, thereby inhibiting the PMN respiratory burst."

"Mercury: god of TH2 cells ?"; Mathieson PW; Clinical Exp Immunol; 102:2:229-30; 1995; Nov;

Review of Literature and Editorial
1. In lower doses, HgCl2 has potent effects on the immune system of rodents..immune stimulation or immunosuppression depending on the strain of animal involved.
2. In susceptible animals HgCl2 induces autoimmunity, with rats of the kidney.
3. Route of exposure unimportant, inhaled mercury vapor produces same autoimmunity as injected HgCl2 in susceptible rats.
4. Preferential activation of Th2 subset of helper T cells.
5. HgCl2 can induce apoptosis in T cells in vitro.
6. HgCl2 induces aggregation of cell surface proteins such as CD4, CD3, CD45 ad Thy-1 on T cells in vitro.
7. Dramatic tyrosine phosphorlation of several cellular proteins...
8. More, very technical effects on intercellular chemicals, compounds etc...
9. Preferential Th2 activation may underlie asthma, allergic disease, and some forms of autoimmunity.

"Immunotoxic effects of mercuric compounds on human lymphocytes and monocytes. Immune Suppression of T-cell activation."; Immunopharmacol Immunotoxical; 14:3, 1992, 539-53; Shenker BJ; Rooney C; Vitale L; Shapiro IM; Department of Pathology, University of Pennsylvania School of Dental Medicine.

Experiment, Findings and Facts
1. T-Cells treated with 0-1000 ng HgCl2, and 0-100 ng CH3HgCl.
2. Both created dose dependent reduction in T-cell proliferation.
3. Presence of monocytes required for reduction. Without, HgCl2 enhanced proliferation of T-cells.
4. CH3HgCl was approximately 5-10 times more potent than HgCl2.
5. Mercury inhibited the ability of these cells to synthesize and secrete IL-1.
6. Decrease in T-cell function indicates mercury-containing compounds are immunotoxic at very low exposure levels.
7. Mercuric compounds have adverse effects on both nuetrophil and macrophage function.
8. Low doses of mercury have a profound inhibitory effect on human T-lymphocyte activation.
9. A high concentration of mercuric ions would be expected to be retained at the cell membrane where they would serve to inactivate enzyme systems, especially those that exhibit free thiol (sulphydral) groups.
10. While immunologic dysfunction has not been considered to be an overt effect of mercury toxicity, it nonetheless may be a critical event.

"Comparison of the interaction of methylmercury and mercuric chloride with murine macrophages"; Arch. Toxicol; 1993; 3:67:205-11; Christensen MM; Ellerman-Eriksen S; RungbyJ; Mogenson SC.

Findings and Facts
1. Macrophage cultures treated with methylmercury resulted in decreased cell viability in a concentration-dependent fashion.
2. Cell viability showed no difference between equimolar concentrations of methylmercury and mercuric chloride.
3. Interferon synthesis was reduced in a concentration dependent manner with either methylmercury or mercuric chloride.
4. Impairment of random migration and phagocytosis appeared with lower concentrations of methylmercury.
5. Electron microscope of methylmercury exposed cells showed mercury deposits in lysosomes, cytoplasm and nuclei.
6. Methylmercury is 100 times more toxic to animals than inorganic mercury, partly due to differences in absorption and solubility.
7. As a result of phagocytic activity, macrophages are often exposed to higher concentrations of toxic metals than other cells.
8. Mercury and cadmium inhibit macrophage release of toxic oxygen species.
9. Mercuric chloride inhibited interferon production at much lower concentrations than migration and phagocytosis.
10. Inorganic mercury appears to move into the cells after damage to the membrane barrier, while methylmercury can penetrate cells without damage to the cell membrane.

"New aspects of murine coxsackie B3 myocarditis--focus on heavy metals"; European Heart Journal; 1995, Dec; Ilblack NG; Lindh U; Fohlman J; Friman G; 16: suppl O; 20-4.

Findings
1. Magnitude of inflammatory lesions in the hearts of coxsackie B3 (CB3)-virus infected mice can be affected by methylmercury.
2. CH3Hg appeared to have a direct effect on immune cells that resulted in changed natural killer cell activity and decreased mobilization of macrophages, CD4+ and CD8+ cells into the inflammatory lesions.
3. Another detrimental effect of CH3Hg treatment was evident by an increased calcium and decreased zinc content in the inflamed heart.
4. CH3Hg increased T-cell activity in the spleen, but the NK-cell activity decreased both in the blood and the spleen.

"In vitro reactions of macrophages to metal ions from dental biomaterials"; Dental Materials; 11:239-245, July 1995; JC Wataha; CT Hanks; Z Sun.

Findings
1. Macrophages react adversely to metal ions at similar concentrations as other cell types found in the oral cavity.
2. Concentrations which affect cell metabolism and protein production are generally lower than those which kill the cell.
3. Non-lethal concentrations of metal ions may alter the secretion of protein inflammatory mediators such as cytokines.

"Murine systemic autoimmune disease induced by mercuric chloride: T helper cells reacting to self proteins."; Int Arch Allergy Immunol; 109:1:11-20 ;1996 Jan; Kubicka-Muranyi M; Kremer J; Rottmann N; Luben B; Albers R; Bloksma N; Luhrmann R; Gleichmann E.

Findings
1. HgCl2 induces a CD4+ T-cell dependent systemic autoimmune disease in susceptible strains of rats and mice.
2. In rats, autoreactive T cells were shown to be involved.
3. In mice attention focused on "Hg-specific" T-cells.
4. T-cells from donors short term exposed to HgCl2 didn't self attack, but mounted a significant reponse to HgCl2 and HgCl2 bearing cells.
5. T-cells from donors long term treated with HgCl2 hardly reacted to HgCl2 and Hg containing spleenic proteins, responding vigorously to nuclei and fibrillarin irrespective of whether these self constituents had been treated with HgCl2 or not.


"Autoreactive T cells in mercury-induced autoimmune disease: in vitro demonstration"; J Immunol, 137:8; 1986 Oct 15, 2548-54; Pelletier L; Pasquier R; Hirsch F; Sapin C; Druet P.

1. Mercuric chloride induces in Brown-Norway rats an autoimmune disease due to a T dependent polyclonal activation of B cells.
2. HgCl2-pretreated cells were injected into the footpads of normal recipients of the same genetic strain.
3. These experiments demonstrate that HgCl2 induces autoreactive T cells, and suggests that these cells may be responsible for the autoimmune disease.




It could be mercury, it could be uranium, who knows?