Environmental factors in autoimmune diseases, February 4–5, 2003, Durham, NC, USA

2003 ◽  
Vol 2 (5) ◽  
pp. 284-289 ◽  
Author(s):  
Vered Molina ◽  
Michael Ehrenfeld
Keyword(s):  
Environmental Factors ◽  
Autoimmune Diseases

scholarly journals Special Issue: Autoimmune Disease Genetics

Genes ◽  
2021 ◽  
Vol 12 (12) ◽  
pp. 1937
Author(s):  
Malgorzata Gabriela Wasniewska ◽  
Artur Bossowski
Keyword(s):  
Autoimmune Disease ◽  
Environmental Factors ◽  
Autoimmune Diseases ◽  
Immunological Tolerance ◽  
Special Issue ◽  
Genetic And Environmental Factors

Autoimmune diseases (ADs) are characterized by a multifactorial etiology, in which genetic and environmental factors are responsible for the loss of immunological tolerance [...]

scholarly journals Dietary Habits Bursting into the Complex Pathogenesis of Autoimmune Diseases: The Emerging Role of Salt from Experimental and Clinical Studies

Nutrients ◽  
2019 ◽  
Vol 11 (5) ◽  
pp. 1013 ◽  
Author(s):  
Rossana Scrivo ◽  
Carlo Perricone ◽  
Alessio Altobelli ◽  
Chiara Castellani ◽  
Lorenzo Tinti ◽  
...  
Keyword(s):  
Environmental Factors ◽  
Autoimmune Diseases ◽  
Lupus Erythematosus ◽  
Clinical Studies ◽  
Dietary Habits ◽  
Salt Intake ◽  
Experimental Models ◽  
Fine Tuning ◽  
Current Evidence

The incidence and prevalence of autoimmune diseases have increased in Western countries over the last years. The pathogenesis of these disorders is multifactorial, with a combination of genetic and environmental factors involved. Since the epidemiological changes cannot be related to genetic background, which did not change significantly in that time, the role of environmental factors has been reconsidered. Among these, dietary habits, and especially an excessive salt, typical of processed foods, has been implicated in the development of autoimmune diseases. In this review, we summarize current evidence, deriving both from experimental models and clinical studies, on the capability of excessive salt intake to exacerbate proinflammatory responses affecting the pathogenesis of immune-mediated diseases. Data on several diseases are presented, including rheumatoid arthritis, systemic lupus erythematosus, multiple sclerosis, and Crohn’s disease, with many of them supporting a proinflammatory effect of salt. Likewise, a hypertonic microenvironment showed similar effects in experimental models both in vivo and in vitro. However, murine models of spontaneous autoimmune polyneuropathy exposed to high salt diet suggest opposite outcomes. These results dictate the need to further analyse the role of cooking salt in the treatment and prevention of autoimmune diseases, trying to shape a fine tuning between the possible advantages of a restricted salt intake and the changes in circulating metabolites, mediators, and hormones which come along salt consumption and could in turn influence autoimmunity.

scholarly journals Xenobiotic Exposure and Autoimmune Hepatitis

2010 ◽  
Vol 2010 ◽  
pp. 1-10 ◽  
Author(s):  
Kathleen M. Gilbert
Keyword(s):  
Environmental Factors ◽  
Autoimmune Diseases ◽  
Autoimmune Hepatitis ◽  
Environmental Pollutants ◽  
Xenobiotic Exposure

Although genetics contributes to the development of autoimmune diseases, it is clear that “environmental” factors are also required. These factors are thought to encompass exposure to certain drugs and environmental pollutants. This paper examines the mechanisms that normally maintain immune unresponsiveness in the liver and discusses how exposure to certain xenobiotics such as trichloroethylene may disrupt those mechanisms and promote autoimmune hepatitis.

scholarly journals Gene/environment interaction and autoimmune disease

2019 ◽  
Author(s):  
Tamia A Harris ◽  
Shai Bel
Keyword(s):  
Environmental Factors ◽  
Autoimmune Diseases ◽  
Disease Onset ◽  
Environment Interaction ◽  
Gene Environment Interaction ◽  
Environmental Interactions ◽  
Gene Environment ◽  
Two Factors ◽  
Exact Etiology ◽  
Genetic And Environmental Factors

Autoimmune diseases are complex illnesses in which the body’s immune system attacks its own healthy tissues. These diseases, which can be fatal, gravely impact the quality of life of those afflicted by them with no cure currently available. The exact etiology of autoimmune diseases is not completely clear. Biomedical research has revealed that both genetic and environmental factors contribute to the development and progression of these diseases. Nevertheless, genetic and environmental factors alone cannot explain a large proportion of cases, leading to the possibility that the two factors interact in driving disease onset. Understanding how genetic and environmental factor influence host physiology in a manner that leads to the development of autoimmune diseases can reveal the mechanisms by which these diseases manifest, and bring us closer to finding a cure for them. In this chapter, we will review the current research of genetic/environmental interactions that contribute to development of autoimmune diseases, with an emphasis on interactions between the host and the multitudes of microbes that inhabit it, the microbiota.

scholarly journals Epigenetic Changes Induced by Maternal Factors during Fetal Life: Implication for Type 1 Diabetes

Genes ◽  
2021 ◽  
Vol 12 (6) ◽  
pp. 887
Author(s):  
Ilaria Barchetta ◽  
Jeanette Arvastsson ◽  
Luis Sarmiento ◽  
Corrado M. Cilio
Keyword(s):  
Dna Methylation ◽  
Type 1 Diabetes ◽  
Environmental Factors ◽  
Autoimmune Diseases ◽  
Epigenetic Mechanism ◽  
Fetal Life ◽  
Epigenetic Changes ◽  
Maternal Factors ◽  
Immune Mediated

Organ-specific autoimmune diseases, such as type 1 diabetes, are believed to result from T-cell-mediated damage of the target tissue. The immune-mediated tissue injury, in turn, is known to depend on complex interactions between genetic and environmental factors. Nevertheless, the mechanisms whereby environmental factors contribute to the pathogenesis of autoimmune diseases remain elusive and represent a major untapped target to develop novel strategies for disease prevention. Given the impact of the early environment on the developing immune system, epigenetic changes induced by maternal factors during fetal life have been linked to a likelihood of developing an autoimmune disease later in life. In humans, DNA methylation is the epigenetic mechanism most extensively investigated. This review provides an overview of the critical role of DNA methylation changes induced by prenatal maternal conditions contributing to the increased risk of immune-mediated diseases on the offspring, with a particular focus on T1D. A deeper understanding of epigenetic alterations induced by environmental stressors during fetal life may be pivotal for developing targeted prevention strategies of type 1 diabetes by modifying the maternal environment.

Genes, epigenetic regulation and environmental factors: Which is the most relevant in developing autoimmune diseases?

2012 ◽  
Vol 11 (8) ◽  
pp. 604-609 ◽  
Author(s):  
Karen H. Costenbader ◽  
Steffen Gay ◽  
Marta E. Alarcón-Riquelme ◽  
Luca Iaccarino ◽  
Andrea Doria
Keyword(s):  
Environmental Factors ◽  
Autoimmune Diseases ◽  
Epigenetic Regulation

Abstract 456: High Salt Induces Pathogenic Th17 Cells and Exacerbates Autoimmune Diseases

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Markus Kleinewietfeld ◽  
Arndt Manzel ◽  
Jens Titze ◽  
Heda Kvakan ◽  
Nir Yosef ◽  
...  
Keyword(s):  
Environmental Factors ◽  
Autoimmune Diseases ◽  
P38 Mapk ◽  
Th17 Cells ◽  
Salt Intake ◽  
Mapk Pathway ◽  
High Salt ◽  
Dietary Salt ◽  
Dietary Salt Intake

There has been a marked increase in the incidence of autoimmune diseases in the last half-century. While the underlying genetic basis of this class of diseases has recently been elucidated implicating predominantly immune response genes1, changes in environmental factors must ultimate be driving this increase. The recently identified population of interleukin (IL)-17 producing CD4+ helper T cells (Th17 cells) play a pivotal role in autoimmune diseases2. Pathogenic IL-23 dependent Th17 cells have been shown to be critical for the development of experimental autoimmune encephalomyelitis (EAE) an animal model for multiple sclerosis (MS) and genetic risk factors associated with MS are related to the IL23/Th17 pathway1, 2. However, little is known regarding the environmental factors that directly influence Th17 cells. Here we show that increased salt (sodium chloride; NaCl) concentrations found under physiological conditions in vivo dramatically boost the induction of murine and human Th17 cells. High salt conditions activates the p38/MAPK pathway involving the tonicity-responsive enhancer binding protein (TonEBP/NFAT5) and the serum- and glucocorticoid-inducible kinase 1 (SGK1) during cytokine-induced Th17 polarization. Gene silencing or chemical inhibition of p38/MAPK, NFAT5 or SGK1 abrogates the high salt induced Th17 cell development. The Th17 cells generated under high salt display a highly pathogenic and stable phenotype as compared to cells differentiated under normal conditions characterized by the up-regulation of the pro-inflammatory cytokines GM-CSF, TNFα and IL-2. Moreover, mice fed with a high salt diet develop a very severe form of EAE in line with increased central nervous system infiltrating and peripherally induced antigen specific Th17 cells. Thus, increased dietary salt intake might represent an environmental risk factor for the development of autoimmune diseases through the induction of pathogenic Th17 cells.

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