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Pectin Enhances Efficacy of Bifidobacterium infantis against Disease Activity in Dextran Sulfate Sodium‐Induced Colitis in Mice
Author(s) -
Kimble Lindsey,
Nguyen Thuy,
Mathison Bridget,
Chew Boon
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.608.21
Probiotics have been proposed as a therapy for inflammatory bowel diseases. Pectin, a prebiotic fiber, may promote the anti‐inflammatory activity of probiotic bacteria. We studied the effects of pectin and Bifidobacterium longum subsp. infantis (Bi) on disease activity and inflammation biomarkers in a dextran sulfate sodium (DSS) murine model of colitis. Female BALB/c mice (6 wk old; n=48) consumed AIN‐93G diet (control) or the same diet supplemented with Bi, Bi+1% pectin, or Bi+3% pectin for 21 d. Colitis was induced via 3% DSS in the drinking water during the last 7 d. Diets were formulated to provide 1‐2x10 9 cfu Bi/day; there was no difference ( P <0.05) in Bi dose, food intake, or body weight between treatments. Disease activity index scores were consistently elevated in the DSS control group on d 16‐21, indicating colitis induction. Supplementation with Bi and pectin delayed the onset of colitis in a dose dependent manner; at time of sacrifice, disease activity scores were lower ( P <0.05) and colon lengths were increased ( P <0.05) following Bi+3% pectin intervention compared to control. Supplementation with Bi and pectin increased ( P <0.05) cecum weights in a dose dependent manner. Interleukins 2 and 4 were elevated ( P <0.05) in colon tissue culture supernatants following Bi+3% pectin intervention, while Bi+1% pectin increased ( P <0.05) glutathione peroxidase and superoxide dismutase activity in red blood cells, indicating anti‐inflammatory activity. Pectin promotes Bi activity against colitis by delaying the onset of disease severity and attenuating inflammation. Supported by the ARC, Washington State University.

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