Autoimmunity caused by xenobiotics

Bigazzi, Pierluigi E.

doi:10.1016/s0300-483x(96)03591-3

Cited by 59 publications

(30 citation statements)

References 56 publications

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“…Cadmium and lead were included for comparison because they both modulate immune responses and are known to be nephrotoxic (12,20,21). Further, cadmium has been reported to induce an autoimmune-like syndrome in experimental animals whereas lead has not (6).…”

Section: Introductionmentioning

confidence: 99%

Pathology of “Toxic Oils” and Selected Metals in the MRL/lpr Mouse

et al. 2001

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The Toxic Oil Syndrome epidemic that occurred in Spain in 1981 and affected nearly 20,000 people was caused by ingestion of oil mixtures that contained analine-denatured rapeseed oil. To date, an animal model in which to identify the actual etiologic agents(s) and to investigate the pathogenesi s of the disease has not been discovered . In this study, the MRL/lpr was used to assess the histopathologica l response of 3 "toxic oils" and 3 metals. The oils tested were a denatured rapeseed oil collected from a family who were affected by the Toxic Oil Syndrome epidemic in Spain (CO756) plus two synthesized oils (RSD and RSA). Female mice, 7 weeks of age, received an undiluted (neat) or a 1:10 diluted dose of each oil; mercury (50 ppm), cadmium (100 ppm), or lead (50 ppm). Half of each group was killed after 5 weeks of exposure and the remaining mice after 10 weeks of exposure. Body and organ weights (liver, kidney, thymus, and spleen) were recorded and selected organs were collected for histopathology. Ten weeks after treatment, body weights (BW) of the cadmium and lead groups were signi cantly suppressed , and the body weight of the CO756-neat group was signi cantly increased compared to their respective controls. Kidney/BW were decreased in the RSA-neat and RSA 1:10 groups after 10 weeks of exposure, and the kidney/BW in the mercury and cadmium groups were increased. Spontaneous developmen t (12 weeks of age) and progression (17 weeks of age) of histopathologica l lesions are described for selected organs examined in the naṏ ve mice as are changes that resulted from exposure to the "toxic oils" and metals. CO756-neat, mercury, and lead suppressed progression of the glomerulonephriti s that normally occurs in the MRL/lpr mouse. Also of interest were lesions that included mononuclea r cuf ng of hepatic bile ducts, progression of the granulomas that formed in the renal glomeruli, vessels in the lymphoid organs that contained tightly packed lymphocytes , and the presence of plasma cells in the thymus. All 3 oils stimulated early developmen t of the lymphoproliferative syndrome characteristic of the MRL/lpr mouse as demonstrated by an increase in the thymus/BW and spleen/BW ratios after 5 weeks of treatment. These data contribute to our knowledge of spontaneou s disease progression in the thymus, spleen, lymph nodes, and kidneys in the MRL/lpr mouse and the effects of 3 different "toxic oils" and metals on the developmen t and progression of those lesions.

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Section: Introductionmentioning

confidence: 99%

Pathology of “Toxic Oils” and Selected Metals in the MRL/lpr Mouse

et al. 2001

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“…lifestyle, infectious agents) are associated with the induction, development, and exacerbation of autoimmunity. Over the past 40 years, epidemiological studies have provided evidence that exposure to certain drugs or environmental agents represent a significant contributing factor for the onset, remission, or severity of autoimmune diseases (see reviews by Bigazzi, 1997;Miller, 2006;IPCS, 2006IPCS, , 2012. Although some of these claims, like silicone breast implants, turned out to be false, they brought attention to the need to have better predictive models to evaluate the potential for induction or exacerbation of autoimmune diseases.…”

Section: Autoimmunitymentioning

confidence: 99%

“…Since the observation by Hoffman in 1945 (reviewed by SarziPuttini et al, 2005) that administration of sulfadiazine often coincided with the development of SLE, over 35 drugs have been implicated in the onset of autoimmune responses and autoimmune-like disease (Bigazzi, 1997;Lee & Chase, 1975;Tan, 1974). The disease is different than its classical spontaneous counterpart.…”

Section: Drug-induced Autoimmunitymentioning

confidence: 99%

A historical perspective of immunotoxicology

Luster

2013

Journal of Immunotoxicology

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An historical perspective of immunotoxicology is presented beginning from early observations in which exposure to workplace environments led to unexpected immune-mediated lung diseases to its eventual evolution as a sub-discipline in toxicology. As with most toxicology disciplines, immunotoxicology originated from concerns by scientists within industry and government as well as medical professionals to limit human exposure to agents that can potentially effect human health. The basis for these concerns originated from laboratory studies in experimental models and clinical observations that suggested certain industrial and agrochemicals, pharmaceuticals and consumer products were capable of inadvertently interacting with the immune system and cause adverse health effects. The types of immunopathologies observed and mechanisms responsible were found to be broad, being dependent upon the physiochemical properties of an agent, exposure route, and target organ/tissue, and included allergic/hypersensitivity responses, immune dysfunction, manifested by suppression or, in rare instances, stimulation, autoimmune or autoimmune-like diseases, and chronic inflammatory disorders.

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“…Autoimmune reactions to xenobiotics may lead to autoimmune responses characterized just by the production of autoantibodies against autoantigens whereas autoimmune diseases are characterized by immune responses against autoantigens resulting in structural and/or functional damage [8]. One example is pemphigus, whose pathophysiology is described elsewhere in this issue [19b].…”

Section: Autoimmune Reactions To Xenobioticsmentioning

confidence: 99%

The Skin: Target Organ in Immunotoxicology of Small-Molecular-Weight Compounds

Sachs¹,

Baron²

2001

Skin Pharmacol Physiol

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Immunotoxicology studies two different effects of xenobiotics: immunosuppression and dysregulation of immune responses leading to hypersensitivity or autoimmunity. The skin is a major target organ of immunotoxicity which is provoked by small-molecular-weight compounds. Methods may be helpful for immunotoxicological investigations and screenings for adverse effects of xenobiotics which are used for diagnosis or studies on the pathophysiology of skin disorders such as allergic contact dermatitis, cutaneous drug-allergic reactions or autoimmune diseases of the skin. Examples include well-designed patch tests, assays involving antigen-presenting cells such as dendritic cells, but also T lymphocytes, basophiles or keratinocytes.

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Autoimmunity caused by xenobiotics

Cited by 59 publications

References 56 publications

Pathology of “Toxic Oils” and Selected Metals in the MRL/lpr Mouse

Pathology of “Toxic Oils” and Selected Metals in the MRL/lpr Mouse

A historical perspective of immunotoxicology

The Skin: Target Organ in Immunotoxicology of Small-Molecular-Weight Compounds

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