The Role of Microbes in Crohn's Disease

• Published in: Clinical infectious diseases Vol. 44; no. 2; pp. 256 - 262
• Main Authors: Eckburg, Paul B., Relman, David A.
• Format: Journal Article
• Language: English
• Published: Chicago, IL The University of Chicago Press 15.01.2007; University of Chicago Press; Oxford University Press
• Subjects: Antibodies; Bacteria; Biological and medical sciences; Crohn disease; Crohn Disease - genetics; Crohn Disease - immunology; Crohn Disease - microbiology; Crohns disease; Gastroenterology. Liver. Pancreas. Abdomen; Genetic Predisposition to Disease; Humans; Immune system; Inflammatory bowel diseases; Intestinal diseases; Intestinal Mucosa - immunology; Medical sciences; Microbiology; Microbiota; Microorganisms; Other diseases. Semiology; Paratuberculosis; Pathogenesis; Pathogens; Stomach. Duodenum. Small intestine. Colon. Rectum. Anus; Tissue samples; Viewpoint; Human; Crohn disease; Symptomatology; Pathogenesis; Mucosa; Digestive diseases; Intestinal disease; Microorganism; Inflammatory disease
• ISSN: 1058-4838; 1537-6591
• DOI: 10.1086/510385

Despite decades of research, the etiology of Crohn's disease (CD) remains unknown. Its pathogenesis may involve a complex interplay between host genetics, immune dysfunction, and microbial or environmental factors. Microorganisms, including pathogens and members of the indigenous microbiota, may initiate or propagate the inflammatory process in CD. The pathogenesis of CD has been difficult to study, owing to the broad spectrum of typically nonspecific clinical manifestations, the complexity of environmental and genetic factors, the lack of an accurate model of disease, and the limitations of microbiological methods. A more useful and relevant paradigm for the etiology of CD might be based on the idea of a pathogenic microbial community profile and might emphasize the role of interactive sets of microbes, rather than the role of individual organisms. We review how microbes may participate in the pathogenesis of CD and how they may inappropriately activate the mucosal immune system in genetically predisposed individuals.