Abstract At the “5th International Meeting on Inflammatory Bowel Diseases selected topics of inflammatory bowel disease (IBD), including the environment, genetics, the gut flora, the cell response and immunomodulation were discussed in order to better understand specific clinical and therapeutic aspects. The incidence of IBD continues to rise, both in lowand in high-incidence areas. It is believed that factors associated with ‘Westernization’may be conditioning the expression of these disorders. The increased incidence of IBD among migrants from low-incidence to high-incidence areas within the same generation suggests a strong environmental influence. The development of genome-wide association scanning (GWAS) technologies has lead to the discovery of more than 100 IBD loci. Some, as the Th 17 pathway genes, are shared between Crohn's disease (CD) and ulcerative colitis (UC), while other are IBD subtype-specific (autophagy genes, epithelial barrier genes). Disease-specific therapies targeting these pathways should be developed. Epigenetic regulation of the inflammatory response also appears to play an important role in the pathogenesis of IBD. The importance of gut flora in intestinal homeostasis and inflammation was reinforced, the concepts of eubiosis and dysbiosis were introduced, and some strategies for reverting dysbiosis to a homeostatic state of eubiosis were proposed. The current status of studies on the human gut microbiota metagenome, metaprotome, and metabolome was also presented. The cell response in inflammation, including endoplasmic reticulum (ER) stress responses, autophagy and inflammasome-dependent events were related to IBD pathogenesis. It was suggested that inflammation-associated ER stress responses may be a common trait in the pathogenesis of various chronic immune and metabolic diseases. How innate and adaptive immunity signaling events can perpetuate chronic inflammation was discussed extensively. Signal transduction pathways provide intracellular mechanisms by which cells respond and adapt to multiple environmental stresses. The identification of these signals has led to a greater mechanistic understanding of IBD pathogenesis and pointed to potentially new therapeutic targets. A critical analysis of clinical trials and of risk-benefit of biological therapy was presented. The problem of Epstein–Barr virus (EBV) and lymphoma in IBD was extensively discussed. Lymphomas can develop in intestinal segments affected by IBD and are in most cases associated with EBV. The reasons of treatment failure were also analyzed both from basic and clinical points of view. Two very interesting presentations on the integration of research and clinical care in the near future closed the meeting. These presentations were focused on macrotrends affecting healthcare delivery and research, and the need to innovate traditional infrastructures to deal with these changing trends as well as new opportunities to accelerate scientific knowledge.

News from the "5th International Meeting on Inflammatory Bowel Diseases" CAPRI 2010.

LATELLA, GIOVANNI;
2010-01-01

Abstract

Abstract At the “5th International Meeting on Inflammatory Bowel Diseases selected topics of inflammatory bowel disease (IBD), including the environment, genetics, the gut flora, the cell response and immunomodulation were discussed in order to better understand specific clinical and therapeutic aspects. The incidence of IBD continues to rise, both in lowand in high-incidence areas. It is believed that factors associated with ‘Westernization’may be conditioning the expression of these disorders. The increased incidence of IBD among migrants from low-incidence to high-incidence areas within the same generation suggests a strong environmental influence. The development of genome-wide association scanning (GWAS) technologies has lead to the discovery of more than 100 IBD loci. Some, as the Th 17 pathway genes, are shared between Crohn's disease (CD) and ulcerative colitis (UC), while other are IBD subtype-specific (autophagy genes, epithelial barrier genes). Disease-specific therapies targeting these pathways should be developed. Epigenetic regulation of the inflammatory response also appears to play an important role in the pathogenesis of IBD. The importance of gut flora in intestinal homeostasis and inflammation was reinforced, the concepts of eubiosis and dysbiosis were introduced, and some strategies for reverting dysbiosis to a homeostatic state of eubiosis were proposed. The current status of studies on the human gut microbiota metagenome, metaprotome, and metabolome was also presented. The cell response in inflammation, including endoplasmic reticulum (ER) stress responses, autophagy and inflammasome-dependent events were related to IBD pathogenesis. It was suggested that inflammation-associated ER stress responses may be a common trait in the pathogenesis of various chronic immune and metabolic diseases. How innate and adaptive immunity signaling events can perpetuate chronic inflammation was discussed extensively. Signal transduction pathways provide intracellular mechanisms by which cells respond and adapt to multiple environmental stresses. The identification of these signals has led to a greater mechanistic understanding of IBD pathogenesis and pointed to potentially new therapeutic targets. A critical analysis of clinical trials and of risk-benefit of biological therapy was presented. The problem of Epstein–Barr virus (EBV) and lymphoma in IBD was extensively discussed. Lymphomas can develop in intestinal segments affected by IBD and are in most cases associated with EBV. The reasons of treatment failure were also analyzed both from basic and clinical points of view. Two very interesting presentations on the integration of research and clinical care in the near future closed the meeting. These presentations were focused on macrotrends affecting healthcare delivery and research, and the need to innovate traditional infrastructures to deal with these changing trends as well as new opportunities to accelerate scientific knowledge.
File in questo prodotto:
Non ci sono file associati a questo prodotto.
Pubblicazioni consigliate

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11697/19506
Citazioni
  • ???jsp.display-item.citation.pmc??? ND
  • Scopus 18
  • ???jsp.display-item.citation.isi??? 19
social impact