title: Lactobacillus rhamnosus GG on rotavirus-induced injury of ileal epithelium in gnotobiotic pigs.
abstract: OBJECTIVE
  The aim of this study was to study the effect of continued Lactobacillus rhamnosus GG strain (LGG) feeding on rotavirus gastroenteritis in the gnotobiotic (Gn) pig model of virulent human rotavirus (HRV) infection.
  
  
  METHODS
  Gn pigs were assigned to treatment groups: mock control, LGG only, HRV only, or LGG plus HRV. Nine days before HRV inoculation (3 days of age), pigs were fed LGG with a daily dose increase of 10-fold from 10³ to 10¹² colony-forming units (CFU). The 10¹² CFU/dose of LGG feeding continued until post-HRV inoculation day (PID) 6. Clinical sign (diarrhea), rotavirus fecal shedding, histopathology of the ileum, adherent junction and tight junction protein expression in the ileal epithelial cells, mucin production in the large and small intestinal contents, and serum cytokine responses from PID 2 to 6 were examined and compared among the treatment groups.
  
  
  RESULTS
  Clinically, the percentage of pigs developing diarrhea, the mean duration of diarrhea, and the mean cumulative fecal scores were lower in the LGG fed pigs compared to the nonfed pigs after HRV inoculation. LGG partially protected ileal epithelium against HRV-induced compensatory increases of the adherent junction protein α-catenin and β-catenin, tight junction protein occludin, claudin-3 and claudin-4, and leak protein claudin-2. LGG promoted mucin production because the mucin levels in the large intestinal contents of the LGG+HRV pigs were significantly higher than the HRV-only pigs on PID 2. Additionally, LGG maintained the anti-inflammatory cytokine transforming growth factor-β level in serum after HRV infection.
  
  
  CONCLUSIONS
  LGG is moderately effective for ameliorating rotavirus diarrhea by partially preventing injuries to the epithelium.
authors.affiliation: *Department of Biomedical Sciences and Pathobiology, Virginia-Maryland Regional College of Veterinary Medicine, Virginia Polytechnic Institute and State University, Blacksburg, VA †Department of Biochemistry, Rush University, Chicago, IL.
authors.forename: Fangning
authors.initials: F
authors.lastname: Liu
authors.forename: Guohua
authors.initials: G
authors.lastname: Li
authors.forename: Ke
authors.initials: K
authors.lastname: Wen
authors.forename: Shaoping
authors.initials: S
authors.lastname: Wu
authors.forename: Yongguo
authors.initials: Y
authors.lastname: Zhang
authors.forename: Tammy
authors.initials: T
authors.lastname: Bui
authors.forename: Xingdong
authors.initials: X
authors.lastname: Yang
authors.forename: Jacob
authors.initials: J
authors.lastname: Kocher
authors.forename: Jun
authors.initials: J
authors.lastname: Sun
authors.forename: Bernard
authors.initials: B
authors.lastname: Jortner
authors.forename: Lijuan
authors.initials: L
authors.lastname: Yuan
mesh_terms: D000818:Animals; D003967:Diarrhea / Q000188:drug therapy* / Q000453:epidemiology / Q000821:virology; D004195:Disease Models, Animal; D005260:Female; D005856:Germ-Free Life; D007082:Ileum / Q000378:metabolism / Q000382:microbiology* / Q000821:virology; D007413:Intestinal Mucosa / Q000378:metabolism / Q000382:microbiology* / Q000821:virology; D007420:Intestine, Large / Q000378:metabolism; D052201:Lacticaseibacillus rhamnosus; D008297:Male; D009077:Mucins / Q000378:metabolism; D015995:Prevalence; D019936:Probiotics / Q000627:therapeutic use*; D011506:Proteins / Q000378:metabolism; D012401:Rotavirus; D012400:Rotavirus Infections / Q000188:drug therapy* / Q000378:metabolism / Q000821:virology; D012720:Severity of Illness Index; D013552:Swine; D016212:Transforming Growth Factor beta / Q000097:blood
chemical_list: D009077:Mucins; D011506:Proteins; D016212:Transforming Growth Factor beta