Probiotic administration alters the gut flora and attenuates colitis in mice administered dextran sodium sulfate.
BACKGROUND
Probiotics are used in the therapy of inflammatory bowel disease. This study aimed to determine whether prior administration of probiotic lactobacilli and bifidobacteria would prevent disease and change gut flora in an animal model of colitis.


METHODS
Swiss albino mice received a probiotic mixture (four Lactobacillus and four Bifidobacterium species) or medium (control) for a week prior to induction of colitis by oral 4% dextran sodium sulfate (DSS) for seven days. Appropriate non-colitis controls were used. Histological damage was assessed (n = 5 per group), as was expression of mRNA for tumor necrosis factor (TNF)-alpha, interferon (IFN)-gamma, transforming growth factor (TGF)-beta1 and SOCS-1 in the colonic mucosa (n = 6 per group). Secretion of TNF-alpha was measured in distal colon organ culture (n = 5-6 per group). Levels of Bacteroides, Bifidobacterium, and Lactobacillus acidophilus in feces were quantified by real time polymerase chain reaction (PCR) targeting 16S rDNA.


RESULTS
Compared to untreated DSS colitis, probiotic treatment significantly reduced weight loss (P < 0.05), shifted histological damage to lesser grades of severity (P < 0.001), reduced mRNA expression of TNF-alpha and TGF-beta1 (P < 0.05), and down-regulated production of TNF-alpha from distal colon explants (P < 0.05). Colitis induced a significant reduction in the relative proportions of Bifidobacterium, Bacteroides and Lactobacillus acidophilus group bacteria in feces, and these levels were significantly increased in probiotic-treated mice compared to DSS mice (P < 0.001).


CONCLUSIONS
Prior administration of probiotic bacteria reduced mucosal inflammation and damage in DSS-induced colitis. DSS colitis was associated with significant changes in the fecal anaerobic bacterial flora and these changes were modulated by administration of probiotic bacteria.
Nanda Kumar
Navalpur S
NS
Department of Gastrointestinal Sciences, The Wellcome Trust Research Laboratory, Christian Medical College, Vellore, India.
Balamurugan
Ramadass
R
Jayakanthan
Kabirdoss
K
Pulimood
Anna
A
Pugazhendhi
Srinivasan
S
Ramakrishna
Balakrishnan S
BS
D000818:Animals; D001439:Bacteroides / Q000254:growth & development; D001644:Bifidobacterium / Q000235:genetics / Q000254:growth & development*; D003092:Colitis / Q000139:chemically induced / Q000276:immunology / Q000382:microbiology / Q000517:prevention & control*; D003106:Colon / Q000276:immunology / Q000382:microbiology* / Q000473:pathology; D016264:Dextran Sulfate; D004195:Disease Models, Animal; D005243:Feces / Q000382:microbiology; D007371:Interferon-gamma / Q000378:metabolism; D007778:Lactobacillus / Q000235:genetics / Q000254:growth & development*; D008297:Male; D051379:Mice; D009924:Organ Culture Techniques; D019936:Probiotics / Q000008:administration & dosage*; D012333:RNA, Messenger / Q000378:metabolism; D012720:Severity of Illness Index; D000071222:Suppressor of Cytokine Signaling 1 Protein; D050826:Suppressor of Cytokine Signaling Proteins / Q000378:metabolism; D053773:Transforming Growth Factor beta1 / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D012333:RNA, Messenger; C491590:Socs1 protein, mouse; D000071222:Suppressor of Cytokine Signaling 1 Protein; D050826:Suppressor of Cytokine Signaling Proteins; D053773:Transforming Growth Factor beta1; D014409:Tumor Necrosis Factor-alpha; D007371:Interferon-gamma; D016264:Dextran Sulfate