Effects of feeding a probiotic preparation (SIM) containing inulin on the severity of colitis and on the composition of the intestinal microflora in HLA-B27 transgenic rats.
An overly aggressive immune response to the intestinal microflora in a genetically susceptible host background has been implicated in the pathogenesis of inflammatory bowel diseases. We measured the impact of a probiotic preparation (SIM) containing inulin on the severity of colitis and on intestinal microflora profiles of HLA-B27-beta(2)-microglobulin transgenic (TG) rats. SIM is a mixture of lactobacilli, bifidobacteria, and inulin. Two-month-old TG rats received either SIM or water. Control TG rats received metronidazole, alone or in combination with SIM, for 8 weeks. Nontransgenic rats received SIM or water. The cecal content was removed for analysis of the intestinal microflora by PCR combined with denaturing gradient gel electrophoresis. The colon was scored for histological evidence of inflammation, colonic myeloperoxidase activity and interleukin-1beta RNA levels were measured photometrically or by real-time quantitative PCR. At 4 months, the colonic inflammation of TG rats treated with SIM was histologically diminished compared to that in untreated TG rats (2.2 +/- 0.2 versus 2.9 +/- 0.1; P </= 0.03). The administration of SIM altered the microflora profiles of TG rats by increasing the diversity and stimulating specifically the growth of Bifidobacterium animalis. The probiotic bacteria added to SIM were below the detection level in cecal stool samples at the end of the study period. The administration of SIM resulted in a measurable impact on the cecal microflora profiles of TG rats with attenuation of colitis. The lack of detection of any added probiotic bacteria in the cecal content suggests that prebiotic inulin is the major effective compound.
Schultz
M
M
Department of Internal Medicine I, University of Regensburg, Regensburg 93042, Germany. michael.schultz@klinik.uni-regensburg.de
Munro
K
K
Tannock
G W
GW
Melchner
I
I
Göttl
C
C
Schwietz
H
H
Schölmerich
J
J
Rath
H C
HC
D000818:Animals; D030801:Animals, Genetically Modified; D001419:Bacteria / Q000235:genetics / Q000302:isolation & purification; D001644:Bifidobacterium / Q000187:drug effects / Q000235:genetics / Q000302:isolation & purification; D003092:Colitis / Q000188:drug therapy* / Q000276:immunology / Q000382:microbiology; D003106:Colon / Q000187:drug effects / Q000378:metabolism / Q000382:microbiology; D004269:DNA, Bacterial / Q000032:analysis; D004591:Electrophoresis, Polyacrylamide Gel; D015796:HLA-B27 Antigen / Q000235:genetics / Q000276:immunology*; D015212:Inflammatory Bowel Diseases / Q000188:drug therapy / Q000382:microbiology / Q000473:pathology; D007422:Intestines / Q000187:drug effects / Q000382:microbiology* / Q000473:pathology; D007444:Inulin / Q000494:pharmacology* / Q000627:therapeutic use; D007778:Lactobacillus / Q000187:drug effects / Q000235:genetics / Q000302:isolation & purification; D007779:Lactobacillus acidophilus / Q000187:drug effects / Q000235:genetics / Q000302:isolation & purification; D008795:Metronidazole / Q000494:pharmacology / Q000627:therapeutic use; D009195:Peroxidase / Q000378:metabolism; D016133:Polymerase Chain Reaction; D019936:Probiotics / Q000494:pharmacology* / Q000627:therapeutic use; D051381:Rats; D011916:Rats, Inbred F344; D017422:Sequence Analysis, DNA; D001613:beta 2-Microglobulin / Q000235:genetics / Q000276:immunology
D004269:DNA, Bacterial; D015796:HLA-B27 Antigen; D001613:beta 2-Microglobulin; D008795:Metronidazole; D007444:Inulin; D009195:Peroxidase