الفهرس 
Introduction and aim of the workOnly 14 pages are availabe for public view
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Abstract
The aim of the present study was to throe light on intestinal expression of TLR4, TLR2 and TLR9 (from the TLRs) and β- defensin-2, β - defensin-3, α- defensin-5, α- defensin-6 (from the defensin family) in inflammatory bowel diseases trying to investigate the role of theses innate immunity elements in the pathogenesis of these enigmatic disorders.
The present study showed that epithelial expression of defensins was predominantly increased in α- defensin-5 and β - defensin-3 in UC, while α- defensin-5 and α- defensin-6 in CD. In UC, decreased expression of β - defensin-2 in colonic epithelial cells was correlated with mucosal inflammation.
In the current study we also demonstrated that TLRS are expressed in human intestinal mucosa. TLR2 expression is mainly stained in mononuclear cells in the mucosa and sub mucosa but almost negative in epithelial cells in UC and CD.
The present study did not confirm epithelial expression of TLR4, but showed some mononuclear cells in the mucosa and sub mucosa did express TLR4.
The study presumed an assumption to the role of innate immunity in IBD: in a genetically susceptible host, alack of the immate defense system represented by decreased β - defensin-2 and -3 induction which provide a first line of defense against potentially pathogenic microbes at the body’s mucosal epithelial frontier may lead to a permanent but slow bacterial invasions triggering the inflammatory process of IBD through the layers of the sub mucosa.
The deferential up regulation of potent β - defensin-3 in the UC epithelial layers may be, in a part, considered one of the distinguishing factors in the pathogenesis of UC and CD.