title: Reduced diversity and increased virulence-gene carriage in intestinal enterobacteria of coeliac children.
abstract: BACKGROUND
  Coeliac disease is an immune-mediated enteropathology triggered by the ingestion of cereal gluten proteins. This disorder is associated with imbalances in the composition of the gut microbiota that could be involved in its pathogenesis. The aim of the present study was to determine whether intestinal Enterobacteriaceae populations of active and non-active coeliac patients and healthy children differ in diversity and virulence-gene carriage, so as to establish a possible link between the pathogenic potential of enterobacteria and the disease.
  
  
  METHODS
  Enterobacteriaceae clones were isolated on VRBD agar from faecal samples of 31 subjects (10 active coeliac patients, 10 symptom-free coeliac patients and 11 healthy controls) and identified at species level by the API 20E system. Escherichia coli clones were classified into four phylogenetic groups A, B1, B2 and D and the prevalence of eight virulence-associated genes (type-1 fimbriae [fimA], P fimbriae [papC], S fimbriae [sfaD/E], Dr haemagglutinin [draA], haemolysin [hlyA], capsule K1 [neuB], capsule K5 [KfiC] and aerobactin [iutA]) was determined by multiplex PCR.
  
  
  RESULTS
  A total of 155 Enterobacteriaceae clones were isolated. Non-E. coli clones were more commonly isolated in healthy children than in coeliac patients. The four phylogenetic E. coli groups were equally distributed in healthy children, while in both coeliac patients most commensal isolates belonged to group A. Within the virulent groups, B2 was the most prevalent in active coeliac disease children, while D was the most prevalent in non-active coeliac patients. E coli clones of the virulent phylogenetic groups (B2+D) from active and non-active coeliac patients carried a higher number of virulence genes than those from healthy individuals. Prevalence of P fimbriae (papC), capsule K5 (sfaD/E) and haemolysin (hlyA) genes was higher in E. coli isolated from active and non-active coeliac children than in those from control subjects.
  
  
  CONCLUSIONS
  This study has demonstrated that virulence features of the enteric microbiota are linked to coeliac disease.
authors.affiliation: Instituto de Agroquímica y Tecnología de Alimentos (CSIC), Apartado 73, 46100 Burjassot, Valencia, Spain. sanest@iata.csic.es
authors.forename: Ester
authors.initials: E
authors.lastname: Sánchez
authors.forename: Inmaculada
authors.initials: I
authors.lastname: Nadal
authors.forename: Ester
authors.initials: E
authors.lastname: Donat
authors.forename: Carmen
authors.initials: C
authors.lastname: Ribes-Koninckx
authors.forename: Miguel
authors.initials: M
authors.lastname: Calabuig
authors.forename: Yolanda
authors.initials: Y
authors.lastname: Sanz
mesh_terms: D018830:Adhesins, Escherichia coli / Q000235:genetics / Q000378:metabolism; D016022:Case-Control Studies; D002446:Celiac Disease / Q000382:microbiology*; D002648:Child; D002675:Child, Preschool; D004755:Enterobacteriaceae / Q000235:genetics* / Q000378:metabolism / Q000472:pathogenicity*; D004926:Escherichia coli / Q000235:genetics* / Q000378:metabolism / Q000472:pathogenicity*; D029968:Escherichia coli Proteins / Q000235:genetics* / Q000378:metabolism; D005243:Feces / Q000382:microbiology; D036781:Fimbriae Proteins / Q000235:genetics / Q000378:metabolism; D016695:Glycosyltransferases / Q000235:genetics / Q000378:metabolism; D006460:Hemolysin Proteins / Q000235:genetics / Q000378:metabolism; D006801:Humans; D007223:Infant; D007422:Intestines / Q000382:microbiology*; D010802:Phylogeny; D018272:Porins / Q000235:genetics / Q000378:metabolism; D014774:Virulence
chemical_list: D018830:Adhesins, Escherichia coli; C465564:Dr adhesin, E coli; D029968:Escherichia coli Proteins; D006460:Hemolysin Proteins; C036507:Hlya protein, E coli; D018272:Porins; C111243:atpG protein, E coli; C063055:fimbrillin; C101637:ymcE protein, E coli; D036781:Fimbriae Proteins; D016695:Glycosyltransferases; C097521:KfiC protein, E coli