Crohn's disease: the case for bacteria

Citation
C. Prantera et Ml. Scribano, Crohn's disease: the case for bacteria, ITAL J GAST, 31(3), 1999, pp. 244-246
Citations number
39
Categorie Soggetti
Gastroenerology and Hepatology
Journal title
ITALIAN JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY
ISSN journal
11258055 → ACNP
Volume
31
Issue
3
Year of publication
1999
Pages
244 - 246
Database
ISI
SICI code
1125-8055(199904)31:3<244:CDTCFB>2.0.ZU;2-P
Abstract
At the present time, there is no convincing indication that Crohn's disease is a bacterial disease, although an association with mycobacteria has been hypothesised for many years. The hypothesis that bacteria could be the cau se, or at least an important concause of Crohn's disease is supported by se veral experimental and clinical observations: animals kept in a germ-free e nvironment fail to develop intestinal inflammation; bacteria are the cause of human and animal intestinal diseases similar to Crohn's disease: luminal content is necessary for causing gut lesions; and, more-over antibiotics a re successfully risen in the treatment of Crohn's disease. Bradford Hill cr iteria recently used to assess a causal relationship for Helicobacter pylor i and peptic ulcer can be applied for establishing or excluding a causality between mycobacteria and Crohn's disease. Of these criteria, only biologic al plausibility coherence and analogy are satisfied. However, failure To id entity a specific pathogen does not exclude a possible role for bacteria in causing Crohn's disease lesions and symptoms. Pathogenic or commensal ente ric bacteria could overinfect the primary lesions, leading to chronic intes tinal inflammation in generically susceptible hosts. Another possibility is that components of the normal intestinal flora could acquire pathogenic ch aracteristics.