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. 2011 Feb;163(2):250-9.
doi: 10.1111/j.1365-2249.2010.04286.x. Epub 2010 Nov 19.

Oral administration of Parabacteroides distasonis antigens attenuates experimental murine colitis through modulation of immunity and microbiota composition

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Oral administration of Parabacteroides distasonis antigens attenuates experimental murine colitis through modulation of immunity and microbiota composition

M Kverka et al. Clin Exp Immunol. 2011 Feb.

Abstract

Commensal bacteria have been shown to modulate the host mucosal immune system. Here, we report that oral treatment of BALB/c mice with components from the commensal, Parabacteroides distasonis, significantly reduces the severity of intestinal inflammation in murine models of acute and chronic colitis induced by dextran sulphate sodium (DSS). The membranous fraction of P. distasonis (mPd) prevented DSS-induced increases in several proinflammatory cytokines, increased mPd-specific serum antibodies and stabilized the intestinal microbial ecology. The anti-colitic effect of oral mPd was not observed in severe combined immunodeficient mice and probably involved induction of specific antibody responses and stabilization of the intestinal microbiota. Our results suggest that specific bacterial components derived from the commensal bacterium, P. distasonis, may be useful in the development of new therapeutic strategies for chronic inflammatory disorders such as inflammatory bowel disease. VSports手机版.

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Figures

Fig. 1
Fig. 1
Pretreatment with membranous fraction of Parabacteroides distasonis (mPd) decreases the dextran sulphate sodium (DSS)-related increase in cytokine production in colon tissue as measured by cytokine antibody array. Values represent the percentage of the intensity of positive control. Granulocyte colony-stimulating factor (G-CSF), interleukin (IL)-l–12p40p70, macrophage inflammatory protein-1α (MIP), stem cell factor (SCF), growth-regulated alpha protein precursor (KC), tissue inhibitor of metalloproteinases-1 (TIMP), tumour necrosis factor-α (TNF), thrombopoietin (TPO) and vascular endothelial growth factor (VEGF). Data are means (bars) and standard deviation (whisker) of three samples [*P < 0·05 versus DSS/phosphate-buffered saline (PBS)].
Fig. 2
Fig. 2
Pretreatment with membranous fraction of Parabacteroides distasonis (mPd) decreases cytokine production (pg/mg of tissue) in different parts of the gut in orally treated BALB/c mice as measured by enzyme-linked immunosorbent assay (ELISA). *P < 0·05 between mPd and phosphate-buffered saline (PBS) (a) or dextran sulphate sodium (DSS)/mPd and DSS/PBS (b)-treated mice. (B.D.) Values below the detection limit; n = 5 mice per group.
Fig. 3
Fig. 3
Oral treatment with membranous fraction of Parabacteroides distasonis (mPd) stabilize the intestinal microbiota without changing the P. distasonis or Bacteroides/Prevotela group stool content. (a) Changes in fecal bacterial populations of dextran sulphate sodium/phosphate-buffered saline (DSS/PBS) and DSS/mPd-treated mice were measured by 16S rRNA gene polymerase chain reaction- denaturing gradient gel electrophoresis (PCR-DGGE) before the treatment day 0 (before colitis induction), day 28 and at the end of the experiment (day 35). (b) Comparison of changes in DGGE profiles between PBS and mPd-treated mice at different time-points. (c) Representative quantitative changes in the Bacteroides/Prevotela group or P. distasonis in stool were measured by quantitative PCR. Data are expressed as a percentage of total Eubacteria[bar (mean); whisker (standard deviation)]. Samples from the same mouse at different time-points were arranged together. The bands marked with arrows were identified as B. acidofaciens, 100% (i), uncultured bacterium related to Clostridium (ii), Lactobacillus johnsonii, 98% and L. gasseri, 98% (iii), H. muridarum, 95% (iv) and Lactobacillus sp. 97% (v) by 16S rRNA sequence analysis.

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