Abstract |
Ulcerative colitis (UC) is a chronic inflammatory disease limited to the colon. Although the pathogenesis of inflammatory bowel disease (IBD) remains unclear, several studies have suggested that the onset and development of IBD require the interaction between genetic susceptibility, stimulation by luminal bacterial antigens and adjuvants, and episodic environmental triggers which break the mucosal barrier. There are many reports that experimental enterocolitis in animals does not occur in a sterile (germ free) environment and is prevented by antibiotics therapy. Moreover, patients with UC exhibit pathological immune responses to many commensal enteric bacterial species. Recent data showed that certain probiotic species decrease relapse of UC. These findings suggest that the most possible cause of UC is associated with chronic intestinal inflammation which is induced and perpetuated by non-pathogenic bacteria in genetically susceptible hosts.
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Authors | Satoko Inoue, Hiroshi Nakase, Tsutomu Chiba |
Journal | Nihon rinsho. Japanese journal of clinical medicine
(Nihon Rinsho)
Vol. 63
Issue 5
Pg. 757-62
(May 2005)
ISSN: 0047-1852 [Print] Japan |
PMID | 15881166
(Publication Type: English Abstract, Journal Article, Review)
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Chemical References |
- Antibodies, Antineutrophil Cytoplasmic
- Cytokines
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Topics |
- Animals
- Antibodies, Antineutrophil Cytoplasmic
- Antibody Formation
- Colitis, Ulcerative
(etiology)
- Colon
(immunology, microbiology)
- Cytokines
- Cytomegalovirus Infections
- Genetic Predisposition to Disease
- Humans
- Immunity, Cellular
- Intestinal Mucosa
(immunology)
- Macrophages
(immunology)
- T-Lymphocytes
(immunology)
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