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A Strong Impact of Genetic Background on Gut Microflora in Mice.

Esworthy RS, Smith DD, Chu FF - Int J Inflam (2010)

Bottom Line: We used diet to modulate ileocolitis; a casein-based defined diet with AIN76A micronutrients (AIN) attenuates inflammation compared to conventional LabDiets.We found that mouse strain had the strongest impact on the composition of microbiota than diet and GPx genotypes.From 129 DKO strictly, we found overgrowth of Escherichia coli.

View Article: PubMed Central - PubMed

Affiliation: Department of Cancer Biology, Beckman Research Institute of the City of Hope, 1500 Duarte Road, Duarte, CA 91010-3000, USA.

ABSTRACT
Genetic background affects susceptibility to ileocolitis in mice deficient in two intracellular glutathione peroxidases, GPx1 and GPx2. The C57BL/6 (B6) GPx1/2 double-knockout (DKO) mice have mild ileocolitis, and 129S1/Sv (129) DKO mice have severe inflammation. We used diet to modulate ileocolitis; a casein-based defined diet with AIN76A micronutrients (AIN) attenuates inflammation compared to conventional LabDiets. Because luminal microbiota induce DKO ileocolitis, we assessed bacterial composition with automated ribosomal intergenic-spacer analysis (ARISA) on cecal DNA. We found that mouse strain had the strongest impact on the composition of microbiota than diet and GPx genotypes. In comparing AIN and LabDiet, DKO mice were more resistant to change than the non-DKO or WT mice. However, supplementing yeast and inulin to AIN diet greatly altered microflora profiles in the DKO mice. From 129 DKO strictly, we found overgrowth of Escherichia coli. We conclude that genetic background predisposes mice to colonization of potentially pathogenic E. coli.

No MeSH data available.


Related in: MedlinePlus

Effect of diet on ileum and colon histology at weaning and peak pathology by strain in GPx1/2-DKO mice. Mice on LabDiet or AIN diet were analyzed at 22 days of age or upon signs of morbidity, and at the peak of ileitis, which is 40 days for B6;129 or 129 N5 and 50 days for B6. 129 N10 mice were only analyzed at 22 days of age due to high morbidity. The AIN diet alleviated ileitis significantly in all strains at both 22 days of age and at peak inflammation (the “∗” sign indicates P < .011). The ileal inflammation/pathology scores increased significantly from 22 days to peak of inflammation in all strains (#P < .034). A diet-associated difference in colitis was only observed in 22-day-old 129 N10 pups (*P < .001).
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fig2: Effect of diet on ileum and colon histology at weaning and peak pathology by strain in GPx1/2-DKO mice. Mice on LabDiet or AIN diet were analyzed at 22 days of age or upon signs of morbidity, and at the peak of ileitis, which is 40 days for B6;129 or 129 N5 and 50 days for B6. 129 N10 mice were only analyzed at 22 days of age due to high morbidity. The AIN diet alleviated ileitis significantly in all strains at both 22 days of age and at peak inflammation (the “∗” sign indicates P < .011). The ileal inflammation/pathology scores increased significantly from 22 days to peak of inflammation in all strains (#P < .034). A diet-associated difference in colitis was only observed in 22-day-old 129 N10 pups (*P < .001).

Mentions: Morbidity at any time appears to be reflection of acute inflammation, reflected in the inflammation/pathology scores of 6 or greater [18]. B6 DKO mice had mean ileal pathology score around 5.5 at 50 days of age, the peak of inflammation in this strain (Figure 2). 129 N10 DKO mice had mean ileal and colonic pathology scores of 6.5 and 9, respectively, at 22 days of age. The pathology scores correlate with morbidity. Typical histopathology in 129 at 22 days of age showed acute inflammation in the cecum and distal colon with frequent skipping or less severe inflammation in the proximal colon (Figure 3). In morbid mice, disease often extended into the proximal colon. By contrast, B6 mice had almost no pathology in the cecum, proximal, and distal colon.


A Strong Impact of Genetic Background on Gut Microflora in Mice.

Esworthy RS, Smith DD, Chu FF - Int J Inflam (2010)

Effect of diet on ileum and colon histology at weaning and peak pathology by strain in GPx1/2-DKO mice. Mice on LabDiet or AIN diet were analyzed at 22 days of age or upon signs of morbidity, and at the peak of ileitis, which is 40 days for B6;129 or 129 N5 and 50 days for B6. 129 N10 mice were only analyzed at 22 days of age due to high morbidity. The AIN diet alleviated ileitis significantly in all strains at both 22 days of age and at peak inflammation (the “∗” sign indicates P < .011). The ileal inflammation/pathology scores increased significantly from 22 days to peak of inflammation in all strains (#P < .034). A diet-associated difference in colitis was only observed in 22-day-old 129 N10 pups (*P < .001).
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2957666&req=5

fig2: Effect of diet on ileum and colon histology at weaning and peak pathology by strain in GPx1/2-DKO mice. Mice on LabDiet or AIN diet were analyzed at 22 days of age or upon signs of morbidity, and at the peak of ileitis, which is 40 days for B6;129 or 129 N5 and 50 days for B6. 129 N10 mice were only analyzed at 22 days of age due to high morbidity. The AIN diet alleviated ileitis significantly in all strains at both 22 days of age and at peak inflammation (the “∗” sign indicates P < .011). The ileal inflammation/pathology scores increased significantly from 22 days to peak of inflammation in all strains (#P < .034). A diet-associated difference in colitis was only observed in 22-day-old 129 N10 pups (*P < .001).
Mentions: Morbidity at any time appears to be reflection of acute inflammation, reflected in the inflammation/pathology scores of 6 or greater [18]. B6 DKO mice had mean ileal pathology score around 5.5 at 50 days of age, the peak of inflammation in this strain (Figure 2). 129 N10 DKO mice had mean ileal and colonic pathology scores of 6.5 and 9, respectively, at 22 days of age. The pathology scores correlate with morbidity. Typical histopathology in 129 at 22 days of age showed acute inflammation in the cecum and distal colon with frequent skipping or less severe inflammation in the proximal colon (Figure 3). In morbid mice, disease often extended into the proximal colon. By contrast, B6 mice had almost no pathology in the cecum, proximal, and distal colon.

Bottom Line: We used diet to modulate ileocolitis; a casein-based defined diet with AIN76A micronutrients (AIN) attenuates inflammation compared to conventional LabDiets.We found that mouse strain had the strongest impact on the composition of microbiota than diet and GPx genotypes.From 129 DKO strictly, we found overgrowth of Escherichia coli.

View Article: PubMed Central - PubMed

Affiliation: Department of Cancer Biology, Beckman Research Institute of the City of Hope, 1500 Duarte Road, Duarte, CA 91010-3000, USA.

ABSTRACT
Genetic background affects susceptibility to ileocolitis in mice deficient in two intracellular glutathione peroxidases, GPx1 and GPx2. The C57BL/6 (B6) GPx1/2 double-knockout (DKO) mice have mild ileocolitis, and 129S1/Sv (129) DKO mice have severe inflammation. We used diet to modulate ileocolitis; a casein-based defined diet with AIN76A micronutrients (AIN) attenuates inflammation compared to conventional LabDiets. Because luminal microbiota induce DKO ileocolitis, we assessed bacterial composition with automated ribosomal intergenic-spacer analysis (ARISA) on cecal DNA. We found that mouse strain had the strongest impact on the composition of microbiota than diet and GPx genotypes. In comparing AIN and LabDiet, DKO mice were more resistant to change than the non-DKO or WT mice. However, supplementing yeast and inulin to AIN diet greatly altered microflora profiles in the DKO mice. From 129 DKO strictly, we found overgrowth of Escherichia coli. We conclude that genetic background predisposes mice to colonization of potentially pathogenic E. coli.

No MeSH data available.


Related in: MedlinePlus