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HLA DQ/DR prevalence and microbiota disturbance in northwestern Mexican children with type 1 diabetes (1118.3)
Author(s) -
MejiaLeon Maria,
Petrosino Joseph,
Ajami Nadim,
DomínguezBello Maria,
Calderon de la Barca Ana
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.1118.3
Subject(s) - bacteroides , prevotella , type 1 diabetes , gut flora , haplotype , medicine , human leukocyte antigen , genetic predisposition , diabetes mellitus , immunology , case control study , biology , allele , disease , genetics , endocrinology , antigen , gene , bacteria
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. Grant Funding Source : Partially Supported by CONACYT grant S0008‐2009‐01‐115212