Genes, bacteria, and immunity contribute to the pathogenesis of inflammatory bowel disease. Most genetic risk relates to defective sensing of microbes and their metabolites or defective regulation of the host response to the microbiota. Because the composition of the microbiota shapes the developing immune system and is determined in early life, the prospect of therapeutic manipulation of the microbiota in adulthood after the onset of disease is questionable. However, the microbiota may be a marker of risk and a modifier of disease activity and a contributor to extraintestinal manifestations and associations in some patients with inflammatory bowel disease.
Key points
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Environmental factors that shape the composition and function of the microbiota are maximally active during the earliest perinatal and postnatal phase of life.
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The neonatal and infant microbiota shapes the development and maturation of the immune system.
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Most of the genetic risk factors for inflammatory bowel disease code for proteins that sense or regulate the host response to the microbiota.
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The molecular mechanisms by which genes, microbes, and the immune system interact in the pathogenesis of inflammatory bowel disease are becoming clarified.
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Strategies for manipulating the microbiota have been remarkably effective in experimental animals but attempts to translate these to the human context have been resoundingly disappointing.
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