Transforming growth factor-beta signaling and matrix metalloproteinase pattern in intestinal strictures in Crohn's disease

Sabatino, Antonio Di; Pickard, Karen; Morera, R.; Cazzola, P.; Corazza, G.R.; MacDonald, T T; Pender, S.

doi:10.1016/s1590-8658(06)80318-x

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“…74,75 The findings of decreased SMAD7 and increased in phosphorylated SMAD2/3 expression observed in intestinal strictures in CD support the profibrogenic role of the TGF-␤/SMAD pathway in CD. 76 Besides the TFG-␤/SMAD pathway, mesenchymal cells, particularly myofibroblasts, appear also to play a role in inflammation-induced fibrosis in the intestine through the action of IGF-1 and TNF-␣, as reported by P.K. Lund (USA).…”

Section: Matrix and Mesenchymal Remodelingmentioning

confidence: 86%

Late-breaking news from the “4th International Meeting on Inflammatory Bowel Diseases” Capri, 2006

Latella

Fiocchi

Caprilli

2007

Inflammatory Bowel Diseases

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At the "4th International Meeting on Inflammatory Bowel Diseases: on the Way to New Therapies," Capri, 2006, genetics, bacteria-host interactions, immunomodulation, and tissue response were discussed deeply in order to understand, rationalize, and develop novel therapies. About genetics, the importance of a better understanding of the nature of known loci and of the putative associations was stressed. It was confirmed that genotype-phenotype associations in inflammatory bowel disease (IBD) have important clinical and therapeutic implications. The importance of the search for dominant bacterial antigens in chronic immune-mediated intestinal inflammation emerged, as well as knowledge of cellular and molecular mechanisms of bacterial-host interactions. It was discussed how innate and adaptive immunity signaling events can perpetuate chronic inflammation. Signal transduction pathways provide an intracellular mechanism by which cells respond and adapt to environmental stress. The identification of these signals have led to a greater understanding of the pathogenesis of IBD and pointed to potential therapeutic targets. It was shown that immune homeostasis is lost in IBD, resulting in a complex tissue response involving the action of immune and nonimmune cells. The nonimmune tissue response in IBD could be regarded as a new target for control of chronic intestinal inflammation. The changing role of biotherapy in IBD was widely discussed and in particular the anti-TNF-alpha monoclonal antibodies. Granulocyte-colony stimulating factor (GM-CSF) and stem cells therapies were also discussed. The risk-to-benefit ratio of the novel therapies was analyzed in detail. Finally, future directions for basic science and the unmet needs for clinical practice were presented.

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Section: Matrix and Mesenchymal Remodelingmentioning

confidence: 86%