title: Toward defining the autoimmune microbiome for type 1 diabetes.
abstract: Several studies have shown that gut bacteria have a role in diabetes in murine models. Specific bacteria have been correlated with the onset of diabetes in a rat model. However, it is unknown whether human intestinal microbes have a role in the development of autoimmunity that often leads to type 1 diabetes (T1D), an autoimmune disorder in which insulin-secreting pancreatic islet cells are destroyed. High-throughput, culture-independent approaches identified bacteria that correlate with the development of T1D-associated autoimmunity in young children who are at high genetic risk for this disorder. The level of bacterial diversity diminishes overtime in these autoimmune subjects relative to that of age-matched, genotype-matched, nonautoimmune individuals. A single species, Bacteroides ovatus, comprised nearly 24% of the total increase in the phylum Bacteroidetes in cases compared with controls. Conversely, another species in controls, represented by the human firmicute strain CO19, represented nearly 20% of the increase in Firmicutes compared with cases overtime. Three lines of evidence are presented that support the notion that, as healthy infants approach the toddler stage, their microbiomes become healthier and more stable, whereas, children who are destined for autoimmunity develop a microbiome that is less diverse and stable. Hence, the autoimmune microbiome for T1D may be distinctly different from that found in healthy children. These data also suggest bacterial markers for the early diagnosis of T1D. In addition, bacteria that negatively correlated with the autoimmune state may prove to be useful in the prevention of autoimmunity development in high-risk children.
authors.affiliation: Department of Microbiology and Cell Science, University of Florida, Gainesville, FL 32611-0700, USA.
authors.forename: Adriana
authors.initials: A
authors.lastname: Giongo
authors.forename: Kelsey A
authors.initials: KA
authors.lastname: Gano
authors.forename: David B
authors.initials: DB
authors.lastname: Crabb
authors.forename: Nabanita
authors.initials: N
authors.lastname: Mukherjee
authors.forename: Luis L
authors.initials: LL
authors.lastname: Novelo
authors.forename: George
authors.initials: G
authors.lastname: Casella
authors.forename: Jennifer C
authors.initials: JC
authors.lastname: Drew
authors.forename: Jorma
authors.initials: J
authors.lastname: Ilonen
authors.forename: Mikael
authors.initials: M
authors.lastname: Knip
authors.forename: Heikki
authors.initials: H
authors.lastname: Hyöty
authors.forename: Riitta
authors.initials: R
authors.lastname: Veijola
authors.forename: Tuula
authors.initials: T
authors.lastname: Simell
authors.forename: Olli
authors.initials: O
authors.lastname: Simell
authors.forename: Josef
authors.initials: J
authors.lastname: Neu
authors.forename: Clive H
authors.initials: CH
authors.lastname: Wasserfall
authors.forename: Desmond
authors.initials: D
authors.lastname: Schatz
authors.forename: Mark A
authors.initials: MA
authors.lastname: Atkinson
authors.forename: Eric W
authors.initials: EW
authors.lastname: Triplett
mesh_terms: D000367:Age Factors; D001323:Autoantibodies / Q000097:blood; D001419:Bacteria / Q000145:classification* / Q000235:genetics / Q000302:isolation & purification; D044822:Biodiversity; D016022:Case-Control Studies; D002648:Child; D002675:Child, Preschool; D003922:Diabetes Mellitus, Type 1 / Q000175:diagnosis / Q000382:microbiology*; D005243:Feces / Q000382:microbiology; D006801:Humans; D007223:Infant; D054892:Metagenome; D012336:RNA, Ribosomal, 16S / Q000235:genetics
chemical_list: D001323:Autoantibodies; D012336:RNA, Ribosomal, 16S