The prevalence of celiac disease (CD) varies greatly, but several reports have shown that CD is increasing in frequency in different geographic areas. The increase in prevalence can be partially attributed to the improvement in diagnostic techniques and disease awareness; however the equally well documented rise in incidence in the last 30-40 years cannot be so easily explained. The new epidemiology of CD is now characterized by an increase of new cases in the historical CD areas (northern Europe and the United States) and more interestingly in a spread of the disease in new regions (Asian countries). A significant change in diet habits, particularly in gluten consumption as well as in infant feeding patterns are probably the main factors that can account for these new trends in CD epidemiology.
[Show abstract][Hide abstract] ABSTRACT: Type 1 Diabetes (T1D) is a pro-inflammatory autoimmune disorder leading to β-cells destruction and insulin deficiency. Its prevalence of 1:300 is increasing and cannot be explained only by HLA DR4-DQ8 and DR3-DQ2 predisposition. Environmental factors seem to have a crucial role in its development through microbiota modulation. The aim of this study was to determine the HLA risk prevalence and to compare the fecal microbiota structure of Mexican children with T1D at onset and after treatment for more than 2 years. A case-control study was conducted in Mexican mestizo children, aged 7-18 years (8 newly diagnosed, 13 controlled T1D cases after 2 years treatment and 8 healthy controls). Predisposing haplotypes were typed and the fecal DNA was extracted; the V4 region of the 16S rRNA gene was amplified and pyrosequenced. All of the T1D cases had at least one HLA risk allele, principally the DQA1*0301. The newly diagnosed T1D cases had high levels of the genus Bacteroides (p<0.004), whereas the control group had a gut microbiota dominated by Prevotella. Children with T1D treated for 蠅2 years had levels of Bacteroides and Prevotella tending to those of the control group. The gut microbiota of newly diagnosed T1D cases is altered, but involving of causes or consequences remains unclear.
The FASEB Journal 04/2014; 28(1):S1118.3. · 5.04 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Abstract Immediately following birth, the gastrointestinal tract is colonized with a complex community of bacteria, which helps shape the immune system. Under conditions of health, the immune system is able to differentiate between innocuous antigens, including food protein and commensals, and harmful antigens such as pathogens. However, patients with celiac disease (CD) develop an intolerance to gluten proteins which results in a pro-inflammatory T-cell mediated immune response with production of anti-gluten and anti-tissue transglutaminase antibodies. This adaptive immune response, in conjunction with activation of innate inflammatory cells, lead to destruction of the small intestinal mucosa. Overall 30% of the global population has genetic risk to develop CD. However, only a small proportion develop CD, suggesting that additional environmental factors must play a role in disease pathogenesis. Alterations in small intestinal microbial composition have recently been associated with active CD, indicating a possible role for the microbiota in CD. However, studies demonstrating causality are lacking. This review will highlight the recent data on the potential role of the microbiota in CD pathogenesis, the potential mechanisms, and discuss future research directions.
Gut Microbes 09/2014; 5(5). DOI:10.4161/19490976.2014.969635
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