The Journal of Pediatrics
Volume 149, Issue 5, Supplement , Pages S107-S114, November 2006

Bacterial colonization, probiotics, and clinical disease

Presented as part of a symposium recognizing the 25th anniversary of the Bristol-Myers Squibb “Freedom to Discover” Nutrition Grants Program, University of Cincinnati, Cincinnati, OH, June 7-8, 2005.

  • Meiqian Weng, MD, PhD
  • ,
  • W. Allan Walker, MD

      Affiliations

    • Corresponding Author InformationReprint requests: W. Allan Walker, MD, Development Gastroenterology Laboratory, Pediatric Gastroenterology and Nutrition Unit, Massachusetts General Hospital for Children, Harvard Medical School, 114 16th Street (114-3405), Charlestown, MA 02129.

From the Development Gastroenterology Laboratory, Pediatric Gastroenterology and Nutrition Unit, Massachusetts General Hospital for Children and Harvard Medical School, Charlestown, MA.

Received 14 April 2006; accepted 1 June 2006.

With the emergence of the hygiene hypothesis, science has begun to reconsider the role of bacteria in host health. Data from germ-free animals and clinical studies support the idea that the colonization of intestinal flora and bacteria-host cross-talk play pivotal roles in the development of the mucosal immune system. Here we discuss the role of commensal colonizing bacteria and toll-like receptor/nucleotide-binding oligomerization domain (TLR/NOD) receptors in the regulation of intestinal immunity and the relationship between TLR/NOD and immune-mediated disease, especially inflammatory bowel disease. We also explore the mechanism of the induction of immune hyporesposiveness by gut epithelial cells interacting with commensal bacteria. A better understanding of bacteria-host interactions will help provide a rational basis for using probiotics as a dietary supplement to prevent and treat disease in the future.

Abbreviations: CAMP, Commensal-associated molecular pattern, CARD, Caspase-activating recruitment domain, CD, Crohn’s disease, DC, Dendritic cell, IBD, Inflammatory bowel disease, IEC, Intestinal epithelial cell, IL, Interleukin, LPS, Lipopolysaccharide, NOD, Nucleotide-binding oligomerization domain, PAMP, Pathogen-associated molecular pattern, Th1, Type 1 helper cell, Th2, Type 2 helper cell, TLR, Toll-like receptor, TNF, Tumor necrosis factor, Treg, Regulator T-cell

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 Dr. Walker is a recipient of a Bristol-Myers Squibb–Mead Johnson Unrestricted Nutrition Research Grant. Mead Johnson sponsored the symposium and provided an honorarium for conference attendance, presentation of the paper, and submission of a manuscript. The authors are entirely and exclusively responsible for its content.

PII: S0022-3476(06)00622-6

doi:10.1016/j.jpeds.2006.06.061

The Journal of Pediatrics
Volume 149, Issue 5, Supplement , Pages S107-S114, November 2006