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Celiac.com 11/28/2014 - According to a new study, obesity plays a major part in triggering and prolonging autoimmune diseases, such as celiac disease, Crohn's disease and multiple sclerosis. The study appeared recently in Autoimmunity Reviews by Prof. Yehuda Shoenfeld, the Laura Schwarz-Kipp Chair for Research of Autoimmune Diseases at Tel Aviv University's Sackler Faculty of Medicine and Head of Zabludowicz Center for Autoimmune Diseases at Chaim Sheba Medical Center, Tel Hashomer. According to the research, obesity erodes the body's ability to protect itself, triggering a pro-inflammatory environment that promotes the development of autoimmune diseases, hastens their progression, and impairs their treatment. For some time now, says Professor Shoenfeld, researchers have been aware of the “negative impact of contributing disease factors, such as infections, smoking, pesticide exposure, lack of vitamins, and the like. But in last five years, a new factor has emerged that cannot be ignored: obesity.” According to the World Health Organization, about one-third of the global population is overweight or obese, nearly a dozen autoimmune diseases are now associated with excess weight, which now impact nearly 5-20% of the global population. That is why, according to Shownfeld, it is “critical to investigate obesity's involvement in the pathology of such diseases." The main culprit is not fat itself, but adipokines, compounds secreted by fat tissue, which impact numerous physiological functions, including the immune response. In tandem with their own study, Shoenfeld and his colleagues reviewed 329 studies from across the globe that focused on the connections between obesity, adipokines, and immune-related conditions like rheumatoid arthritis, multiple sclerosis, type-1 diabetes, psoriasis, inflammatory bowel disease, psoriatic arthritis, and Hashimoto thyroiditis. "According to our study and the clinical and experimental data reviewed, the involvement of adipokines in the pathogenesis of these autoimmune diseases is clear," says Shoenfeld. "We were able to detail the metabolic and immunological activities of the main adipokines featured in the development and prognosis of several immune-related conditions." One of the team’s more interesting findings was that obesity also promotes vitamin D deficiency, which, “once corrected, alleviated paralysis and kidney deterioration associated with the disorder… [and] improved the prognosis and survival of the mice.” Source: Science Daily, November 10, 2014
Celiac.com 11/21/2011 - Celiac disease is common in people with type 1 diabetes (T1D). These people can show Abs reactions against tissue transglutaminase, the prime trigger in celiac disease. In short, gliadin seems to play a role in type 1 diabetes pathogenesis. An international research team set out to investigate whether gliadin contributes to enteropathy and insulitis in NOD-DQ8 mice, an animal model that does not spontaneously develop T1D. The researchers included Heather J. Galipeau, Nestor E. Rulli, Jennifer Jury, Xianxi Huang, Romina Araya, Joseph A. Murray, Chella S. David, Fernando G. Chirdo, Kathy D. McCoy, and Elena F. Verdu, and are variously affiliated with the Farncombe Family Digestive Health Research Institute at McMaster University Medical Centre in Canada, Laboratorio de Investigación en el Sistema Inmune, Departamento de Ciencias Biológicas, Facultad de Ciencias Exactas, Universidad Nacional de La Plata, Argentina, the Department of Internal Medicine, and the Department of Immunology at the Mayo Clinic College of Medicine in Rochester, MN, and with the Department of Clinical Research, University of Bern, Bern, Switzerland. Researchers know that gliadin-sensitized NOD-DQ8 mice develop moderate enteropathy, intraepithelial lymphocytosis, and barrier dysfunction, but do not develop insulitis. The team administered anti-CD25 mAbs before gliadin-sensitization induced partial depletion of CD25+Foxp3+ T cells, which triggered severe insulitis, but did not worsen mucosal dysfunction. The team isolated CD4+ T cells isolated from pancreatic lymph nodes. Those from mice that developed insulitis showed higher proliferation and pro-inflammatory cytokines after incubation with gliadin, but not with BSA. CD4+ T cells isolated from non-sensitized control mice showed no response to gliadin or BSA. From these observations, the team concluded that gliadin sensitization triggered moderate enteropathy in NOD-DQ8 mice. However, triggering insulitis required gliadin-sensitization and partial systemic depletion of CD25+Foxp3+ T cells. This study offers a model for explaining how mucosal intolerance to a dietary protein can trigger insulitis as a result of partial regulatory T cell deficiency. Source: J Immunol. 2011 Oct 15;187(8):4338-46.