Enterotoxigenic Bacteroides fragilis: A potential instigator of colitis

Shervin Rabizadeh, Ki Jong Rhee, Shaoguang Wu, David Huso, Christine M. Gan, Jonathan E. Golub, Xinqun Wu, Ming Zhang, Cynthia L. Sears

Research output: Contribution to journalArticle

58 Citations (Scopus)

Abstract

Background: Inflammatory bowel disease (IBD) is proposed to result from a dysregulated mucosal immune response to the colonic flora in genetically susceptible individuals. Enterotoxigenic Bacteroides fragilis (ETBF), a molecular subclass of the common human commensal, B. fragilis, has been associated with IBD. This study investigated whether ETBF colonization of mice initiated colitis or modified the clinical course of a colitis agonist, dextran sodium sulfate (DSS). Methods: Four- and 6-week-old C57BL/6 mice were inoculated with buffer, nontoxigenic B. fragilis (NTBF) strain 9343(pFD340), or ETBF strain 86-5443-2-2 via orogastric tube. A subset of mice received 2% DSS several days pre- or post-inoculation of bacteria. Clinical status was assessed throughout the experiment and severity of colonic inflammation was scored after sacrifice. Results: AU mice, including those receiving DSS, were clinically well prior to bacterial inoculation. NTBF and ETBF colonization was similar. Regardless of mouse age or timing of DSS administration, mice who received ETBF+DSS experienced worse colitis reflected by less weight gain, enhanced gross disease, and greater inflammation in their colons (P < 0.05), especially in the cecum. In particular, younger mice had more extensive disease. Mice inoculated only with ETBF also exhibited colitis with more severe inflammation when compared to all other groups (P < 0.05) except the ETBF+DSS group. Conclusions: ETBF, a colonic commensal, alone stimulates colitis and significantly enhances colonic inflammation in DSS-treated mice. This study suggests that acquisition of ETBF colonization may be a potential factor in initiation and/or exacerbation of colitis.

Original languageEnglish
Pages (from-to)1475-1483
Number of pages9
JournalInflammatory Bowel Diseases
Volume13
Issue number12
DOIs
Publication statusPublished - 2007 Dec 1

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Bacteroides fragilis
Colitis
Dextran Sulfate
Inflammation
Inflammatory Bowel Diseases
Peptide Initiation Factors
Mucosal Immunity
Cecum
Inbred C57BL Mouse
Weight Gain
Buffers
Colon

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Gastroenterology

Cite this

Rabizadeh, S., Rhee, K. J., Wu, S., Huso, D., Gan, C. M., Golub, J. E., ... Sears, C. L. (2007). Enterotoxigenic Bacteroides fragilis: A potential instigator of colitis. Inflammatory Bowel Diseases, 13(12), 1475-1483. https://doi.org/10.1002/ibd.20265
Rabizadeh, Shervin ; Rhee, Ki Jong ; Wu, Shaoguang ; Huso, David ; Gan, Christine M. ; Golub, Jonathan E. ; Wu, Xinqun ; Zhang, Ming ; Sears, Cynthia L. / Enterotoxigenic Bacteroides fragilis : A potential instigator of colitis. In: Inflammatory Bowel Diseases. 2007 ; Vol. 13, No. 12. pp. 1475-1483.
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Rabizadeh, S, Rhee, KJ, Wu, S, Huso, D, Gan, CM, Golub, JE, Wu, X, Zhang, M & Sears, CL 2007, 'Enterotoxigenic Bacteroides fragilis: A potential instigator of colitis', Inflammatory Bowel Diseases, vol. 13, no. 12, pp. 1475-1483. https://doi.org/10.1002/ibd.20265

Enterotoxigenic Bacteroides fragilis : A potential instigator of colitis. / Rabizadeh, Shervin; Rhee, Ki Jong; Wu, Shaoguang; Huso, David; Gan, Christine M.; Golub, Jonathan E.; Wu, Xinqun; Zhang, Ming; Sears, Cynthia L.

In: Inflammatory Bowel Diseases, Vol. 13, No. 12, 01.12.2007, p. 1475-1483.

Research output: Contribution to journalArticle

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T1 - Enterotoxigenic Bacteroides fragilis

T2 - A potential instigator of colitis

AU - Rabizadeh, Shervin

AU - Rhee, Ki Jong

AU - Wu, Shaoguang

AU - Huso, David

AU - Gan, Christine M.

AU - Golub, Jonathan E.

AU - Wu, Xinqun

AU - Zhang, Ming

AU - Sears, Cynthia L.

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Y1 - 2007/12/1

N2 - Background: Inflammatory bowel disease (IBD) is proposed to result from a dysregulated mucosal immune response to the colonic flora in genetically susceptible individuals. Enterotoxigenic Bacteroides fragilis (ETBF), a molecular subclass of the common human commensal, B. fragilis, has been associated with IBD. This study investigated whether ETBF colonization of mice initiated colitis or modified the clinical course of a colitis agonist, dextran sodium sulfate (DSS). Methods: Four- and 6-week-old C57BL/6 mice were inoculated with buffer, nontoxigenic B. fragilis (NTBF) strain 9343(pFD340), or ETBF strain 86-5443-2-2 via orogastric tube. A subset of mice received 2% DSS several days pre- or post-inoculation of bacteria. Clinical status was assessed throughout the experiment and severity of colonic inflammation was scored after sacrifice. Results: AU mice, including those receiving DSS, were clinically well prior to bacterial inoculation. NTBF and ETBF colonization was similar. Regardless of mouse age or timing of DSS administration, mice who received ETBF+DSS experienced worse colitis reflected by less weight gain, enhanced gross disease, and greater inflammation in their colons (P < 0.05), especially in the cecum. In particular, younger mice had more extensive disease. Mice inoculated only with ETBF also exhibited colitis with more severe inflammation when compared to all other groups (P < 0.05) except the ETBF+DSS group. Conclusions: ETBF, a colonic commensal, alone stimulates colitis and significantly enhances colonic inflammation in DSS-treated mice. This study suggests that acquisition of ETBF colonization may be a potential factor in initiation and/or exacerbation of colitis.

AB - Background: Inflammatory bowel disease (IBD) is proposed to result from a dysregulated mucosal immune response to the colonic flora in genetically susceptible individuals. Enterotoxigenic Bacteroides fragilis (ETBF), a molecular subclass of the common human commensal, B. fragilis, has been associated with IBD. This study investigated whether ETBF colonization of mice initiated colitis or modified the clinical course of a colitis agonist, dextran sodium sulfate (DSS). Methods: Four- and 6-week-old C57BL/6 mice were inoculated with buffer, nontoxigenic B. fragilis (NTBF) strain 9343(pFD340), or ETBF strain 86-5443-2-2 via orogastric tube. A subset of mice received 2% DSS several days pre- or post-inoculation of bacteria. Clinical status was assessed throughout the experiment and severity of colonic inflammation was scored after sacrifice. Results: AU mice, including those receiving DSS, were clinically well prior to bacterial inoculation. NTBF and ETBF colonization was similar. Regardless of mouse age or timing of DSS administration, mice who received ETBF+DSS experienced worse colitis reflected by less weight gain, enhanced gross disease, and greater inflammation in their colons (P < 0.05), especially in the cecum. In particular, younger mice had more extensive disease. Mice inoculated only with ETBF also exhibited colitis with more severe inflammation when compared to all other groups (P < 0.05) except the ETBF+DSS group. Conclusions: ETBF, a colonic commensal, alone stimulates colitis and significantly enhances colonic inflammation in DSS-treated mice. This study suggests that acquisition of ETBF colonization may be a potential factor in initiation and/or exacerbation of colitis.

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