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“Happy is he who has been able to learn the causes of things”Virgil, Georgics II: 490Unfortunately Virgil would not have described us,researchers of today, as happy, because a definitive expla-nation of the causes of Crohn’s disease (CD) is not known. Inthe opinion of some gastroenterologists, inflammatory boweldiseases form a mechanistic continuum that comprises, onone side Ulcerative colitis (UC) and, on the other side, CD[1]. But CD itself is not a single entity because wide varia-tion is seen in anatomic location/extent, disease behaviour,intestinal and extraintestinal manifestations, and response totherapy.Following the most accepted hypothesis, CD happens as aresult of an inappropriate mucosal immune response to ubiq-uitousenvironmentalfactorssuchasintestinalmicrofloraandalimentaryantigensingeneticallysusceptibleindividuals[1].The gene CARD15 or NOD2, associated with CD suscepti-bility, encodes an intracellular receptor involved in the host’sinnate immune system and the response to bacteria [2]. Thisdiscovery strengthens the prominent role of bacteria, amongthe other factors, in causing CD [3].Many other genes are probably involved, and thoserecently discovered interfere with further inflammatorymechanisms. The interactions among different genes andvarious environmental factors account for the difference inlocation, disease behaviour, symptoms, and response to ther-apy. Given all these facts the hypothesis that CD is caused bya single environmental agent is pretty weak.At this point one acceptable question that advocates of themycobacterial hypothesis should ask is if it is possible thatsomecasesclassifiedasCDaremycobacterialdisease.Manytypesofatypicalmycobacteriaexist:someofthemaresapro-phytic; some others are possibly cause of disease in humans,particularly in immunosuppressed patients [4]. Among these |
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