Enhancement of Ovalbumin-induced Antibody Production and Mucosal Mast Cell Response by Mercury

Watzl, Bernhard; Abrahamse, S.L.; Lishaut, S. Treptow-van; Neudecker, C.; Hänsch, Gertrud Maria; Rechkemmer, Gerhard; Pool‐Zobel, Beatrice L.

doi:10.1016/s0278-6915(99)00035-6

Cited by 12 publications

(15 citation statements)

References 37 publications

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“…Although the exact mechanism underlying this effect is unknown, it seems likely that under the inflammatory conditions associated with exposure to mercury and collagen together, mercury acts as an additional adjuvant that preferentially enhances the production of anti‐collagen II IgG2a. This suggestion is supported by findings that mercury exerts adjuvant effects on the specific humoral (IgG) immune responses exhibited by rats immunized with ovalbumin 35 and by mice immunized with horse erythrocytes 36 …”

Section: Discussionmentioning

confidence: 74%

Exposure to mercuric chloride during the induction phase and after the onset of collagen‐induced arthritis enhances immune/autoimmune responses and exacerbates the disease in DBA/1 mice

et al. 2005

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Summary In susceptible mice, mercuric chloride induces a systemic autoimmune response that is characterized by elevated serum levels of immunoglobulin G1 (IgG1) and immunoglobulin E (IgE), production of anti‐nucleolar antibodies (ANolAs) and the formation of renal IgG deposits. We have previously shown that mercury can also enhance immune/autoimmune responses in mouse strains genetically prone to develop spontaneous autoimmune disease. Here, we investigated whether mercury can enhance the severity of murine collagen‐induced arthritis (CIA), an inducible (acquired) autoimmune disease that cannot be induced by mercury itself. While mercury administered prior to the induction phase of CIA exerted little, if any, influence, administration of mercury during the induction phase and following onset aggravated the symptoms of this disease and increased the serum levels of IgE and IgG2a antibodies directed against collagen type II (CII). Furthermore, while animals injected with mercury alone exhibited a significant decrease in the ratio of the levels of interferon‐γ (IFN‐γ) to interleukin‐4 (IL‐4) mRNA in their spleens, this ratio was increased in mice with CIA, with or without administration of mercury. Finally, the production of anti‐nuclear antibodies, a hallmark of autoimmunity in response to mercury, was observed in all mice with CIA treated with this heavy metal. Our findings suggest that exposure to mercury during the development of CIA may influence immunological factors in such a way as to synergistically promote disease development.

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Section: Discussionmentioning

confidence: 74%

Exposure to mercuric chloride during the induction phase and after the onset of collagen‐induced arthritis enhances immune/autoimmune responses and exacerbates the disease in DBA/1 mice

et al. 2005

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“…In rats, multiple exposures to HgCl 2 stimulated the immune response against food allergens, likely via toxicity to lymph node cells (Watzl et al, 1999). Thus, Hg disruption of processes/proteins that are essential for cell functions (e.g., calcium homeostasis, organelles) could potentially lead to immune-cell degeneration and/or toxicity.…”

Section: Hg-induced Immunotoxicity In Mammalian Speciesmentioning

confidence: 99%

Toxicology and Immunotoxicology of Mercury: A Comparative Review in Fish and Humans

Sweet¹,

Zelikoff²

2001

Journal of Toxicology and Environmental Health Part B: Critical Reviews

206

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This review addresses an important area of environmental and mammalian toxicology by evaluating and comparing mercury-induced effects upon the immune responses of two evolutionarily divergent yet immunologically-related species. The mechanisms of mercury toxicology and immunotoxicology are described herein, including supporting data from the following: sources of exposure; bioavailability and biodistribution; metabolism; and laboratory and field investigations. Based upon the studies presented, the relative sensitivities of fish and human immune cells to mercury exposure are compared and contrasted with regard to mercury's ability to stimulate and/or suppress host immunocompetence. In addition, results from immune assays are compared to mercury tissue burdens, as well as to toxicological threshold level estimates. Such comparisons may help to resolve gaps in our knowledge regarding sensitivity of immunological assays, standardization of immunotoxicological techniques between species, and the extent to which the vertebrate immune system possesses functional reserve and redundancy in response to xenobiotics. A review of this type begins to provide support for the potential usefulness of fish immune cells to serve as indicators for human immunotoxicology risk assessment. Analysis of the reviewed studies supports the following conclusions in both lower and higher vertebrates: a threshold for mercury-induced immunotoxicological effects is likely; multiple exposure scenarios involving high and/or chronic exposures leading to increased body burdens are linked to increased risk of immunomodulation; and highly exposed and/or susceptible subpopulations are at greater risk of toxicological impact.

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“…Anti-OVA antibody serum levels were measured by ELISA as reported earlier (Watzl et al 1999a). Briefly, microtitre plates (Maxisorp; NUNC, Roskilde, Denmark) were coated with 50 ml per well of an OVA solution (20 mg/ml).…”

Section: Detection Of Specific Anti-ovalbumin Immunoglobulins E and Gmentioning

confidence: 99%

Dietary wheat germ agglutinin modulates ovalbumin-induced immune responses in Brown Norway rats

Watzl¹,

Neudecker²,

Hänsch

et al. 2001

Br J Nutr

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The trend towards an increased consumption of minimally processed plant food results in a higher intake of non-nutritive compounds such as lectins. Lectins are typically globular proteins that are resistant to digestion in the gastrointestinal tract. They affect the integrity of the intestinal epithelium and the absorption of dietary antigens, and induce the release of allergic mediators from mast cells in vitro. Based on this information we have studied whether dietary wheat germ agglutinin (WGA) could be involved in triggering food allergies. Brown Norway rats were immunized intraperitoneally using ovalbumin (OVA; 10 mg/rat) and 10 d later treated for five consecutive days with WGA (10 mg/rat per d) administered intragastrically. Rats were then orally challenged with OVA (100 mg/rat) 1 h after the last WGA application, and blood was collected 4 h later. Immunological responses (anti-OVA immunoglobulins E and G, rat mast cell protease II, interferon-g and lymphocyte proliferation) were measured and lymphocyte subpopulations were determined. In immunized rats WGA treatment resulted in increased serum rat mast cell protease II concentrations (pre-challenge 0´26 (SE 0´08) mg/ml, post-challenge 0´49 (SE 0´09) mg/ml; P , 0´01) 4 h after the OVA challenge. After 5 d serum concentrations of anti-OVA immunoglobulin E were significantly increased only in the immunized controls (absorbance at 405 nm on days 14 and 19 was 0´09 (SE 0´008) and 0´24 (SE 0´046) respectively; P 0´02), while in WGA-treated rats no significant increase was seen (0´08 (SE 0´004) and 0´15 (SE 0´037 respectively; P 0´14). CD4 + : CD8 +

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Enhancement of Ovalbumin-induced Antibody Production and Mucosal Mast Cell Response by Mercury

Cited by 12 publications

References 37 publications

Exposure to mercuric chloride during the induction phase and after the onset of collagen‐induced arthritis enhances immune/autoimmune responses and exacerbates the disease in DBA/1 mice

Exposure to mercuric chloride during the induction phase and after the onset of collagen‐induced arthritis enhances immune/autoimmune responses and exacerbates the disease in DBA/1 mice

Toxicology and Immunotoxicology of Mercury: A Comparative Review in Fish and Humans

Dietary wheat germ agglutinin modulates ovalbumin-induced immune responses in Brown Norway rats

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