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Loss of intestinal immune regulation leading to aberrant immune responses to the commensal microbiota are believed to precipitate the chronic inflammation observed in the gastrointestinal tract of patients with inflammatory bowel diseases (IBD), Crohn's disease and ulcerative colitis. Innate immune receptors that recognize conserved components derived from the microbiota are widely expressed by both epithelial cells and leucocytes of the gastrointestinal tract and play a key role in host protection from infectious pathogens; yet precisely how pathogenic and commensal microbes are distinguished is not understood. Furthermore, aberrant innate immune activation may also drive intestinal pathology, as patients with IBD exhibit extensive infiltration of innate immune cells to the inflamed intestine, and polymorphisms in many innate immunity genes influence susceptibility to IBD. Thus, a balanced interaction between the microbiota and innate immune activation is required to maintain a healthy mutualistic relationship between the microbiota and the host, which when disturbed can result in intestinal inflammation.

Original publication

DOI

10.1159/000330913

Type

Journal article

Journal

J Innate Immun

Publication Date

2011

Volume

3

Pages

585 - 593

Keywords

Animals, Bacterial Infections, Cell Movement, Genetic Predisposition to Disease, Homeostasis, Humans, Immunity, Innate, Inflammation, Inflammatory Bowel Diseases, Intestinal Mucosa, Lymphocytes, Polymorphism, Genetic