Evidence for the involvement of infectious agents in the pathogenesis of Crohn's disease

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Evidence

for the involvement of infectious agents in the pathogenesis of Crohn’s

disease

Gert De Hertogh, Jeroen Aerssens, P Geboes, and Karel

Geboes

Gert De Hertogh, Karel Geboes, Department of Pathology,

University Hospitals KULeuven, Minderbroedersstraat 12, Leuven 3000, Belgium

Jeroen Aerssens, Tibotec bvba, Generaal De Wittelaan L 11B 3,

Mechelen 2800, Belgium

Karel P Geboes, Department of Gastroenterology, University

Hospitals KULeuven, Herestraat 49, Leuven 3000, Belgium

Correspondence to: Dr. Karel Geboes, UZ Leuven, Dienst

Morfologie & Moleculaire Pathologie, Minderbroedersstraat 12, Leuven 3000,

Belgium. karel.geboes@...

Telephone: +32-16336584

Fax: +32-16336548

Received

October 31, 2007; Revised December 24, 2007

This

article has been cited by other articles in PMC.

Abstract

Many advances have been made in the

understanding of Crohn’s disease (CD) pathogenesis during the last

decade. CD is currently seen as a predominantly T-lymphocyte-driven disease

characterized by the presence of a complex cocktail of interacting cytokines,

chemokines and other mediators produced by a variety of cell types. Prevailing

theories of CD pathogenesis suggest that patients’ T-lymphocytes are

inappropriately activated in the setting of an immune imbalance, which is

itself caused by an unfortunate confluence of genetic and environmental

factors. The T-cell response then leads to the chronic inflammation characteristic

for the disease. Various environmental factors may play a role in the

development of CD, but microbes are most consistently implied. This theory is

based on epidemiological, clinicopathological, genetic and experimental

evidence. Despite the abundance of arguments for the implication of bacteria in

the etiopathogenesis of CD, the precise role of bacteria in this disease still

remains elusive. Three not necessarily mutually exclusive theories have been

proposed: (1) an unidentified persistent pathogen; (2) an abnormally permeable

mucosal barrier leading to excessive bacterial translocation; and (3) a

breakdown in the balance between putative “protective” versus

“harmful” intestinal bacteria (“dysbiosis”). At present,

one cannot exclude with certainty any of these three proposed hypotheses; they

may all apply to CD to a certain extent.

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>

> Evidence for the involvement of infectious agents in the pathogenesis of

Crohn's disease

> Gert De Hertogh, Jeroen Aerssens, P Geboes... etc., etc., etc...