title: Probiotics are effective for the prevention and treatment of Citrobacter rodentium-induced colitis in mice.
abstract: BACKGROUND
  Probiotics prevent disease induced by Citrobacter rodentium, a murine-specific enteric pathogen. Whether probiotics can be used to interrupt the infectious process following initiation of infection was determined.
  
  
  METHODS
  C57BL/6 adult and neonatal mice were challenged with C. rodentium, and a probiotic mixture containing Lactobacillus helveticus and Lactobacillus rhamnosus was provided 1 week before bacterial challenge, concurrently with infection, or 3 days and 6 days after infection. Mice were sacrificed 10 days after infection, and disease severity was assessed by histological analysis and in vivo intestinal permeability assay. Inflammatory pathways and the composition of the fecal microbiome were assessed in adult mice.
  
  
  RESULTS
  Preadministration and coadministration of probiotics ameliorated C. rodentium-induced barrier dysfunction, epithelial hyperplasia, and binding of the pathogen to host colonocytes in adults, with similar findings in neonatal mice. Upregulated tumor necrosis factor α and interferon γ transcripts were suppressed in the pretreated probiotic group, whereas interleukin 17 transcription was suppressed with probiotics given up to 3 days after infection. Probiotics promoted transcription of interleukin 10 and FOXP3, and increased follicular T-regulatory cells in pretreatment mice. C. rodentium infection resulted in an altered fecal microbiome, which was normalized with probiotic intervention.
  
  
  CONCLUSIONS
  This study provides evidence that probiotics can prevent illness and treat disease in an animal model of infectious colitis.
authors.affiliation: Research Institute, Hospital for Sick Children, University of Toronto, Canada.
authors.forename: David M
authors.initials: DM
authors.lastname: Rodrigues
authors.forename: Andrew J
authors.initials: AJ
authors.lastname: Sousa
authors.forename: Kathene C
authors.initials: KC
authors.lastname: Johnson-Henry
authors.forename: Philip M
authors.initials: PM
authors.lastname: Sherman
authors.forename: Mélanie G
authors.initials: MG
authors.lastname: Gareau
mesh_terms: D000818:Animals; D044082:Citrobacter rodentium / Q000254:growth & development* / Q000378:metabolism; D003092:Colitis / Q000378:metabolism / Q000382:microbiology / Q000628:therapy*; D003106:Colon / Q000378:metabolism / Q000382:microbiology; D004756:Enterobacteriaceae Infections / Q000378:metabolism / Q000382:microbiology / Q000628:therapy*; D005243:Feces / Q000382:microbiology; D005260:Female; D051858:Forkhead Transcription Factors / Q000378:metabolism; D006965:Hyperplasia / Q000378:metabolism / Q000382:microbiology / Q000517:prevention & control / Q000628:therapy; D007371:Interferon-gamma / Q000378:metabolism; D016753:Interleukin-10 / Q000378:metabolism; D020381:Interleukin-17 / Q000378:metabolism; D007413:Intestinal Mucosa / Q000378:metabolism / Q000382:microbiology; D052198:Lactobacillus helveticus; D052201:Lacticaseibacillus rhamnosus; D054892:Metagenome; D051379:Mice; D008810:Mice, Inbred C57BL; D019936:Probiotics / Q000494:pharmacology*; D050378:T-Lymphocytes, Regulatory / Q000378:metabolism / Q000382:microbiology; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D051858:Forkhead Transcription Factors; C498833:Foxp3 protein, mouse; D020381:Interleukin-17; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D007371:Interferon-gamma