Attilio Ignazio Lo Monte, Francesca Rappa, Francesco Damiani, Emanuele Sinagra, Giovanni Tomasello, Claudia Campanella, Antonella Marino Gammazza, Francesco Cappello, Alida Abruzzo, Claudia Campanella, A. Marino Gammazza, Maurizio Bellavia, Provvidenza Damiani, Rappa, Luca Cicero, Alida Abruzzo, Tomasello, Damiani, Attilio Ignazio Lo Monte, Cappello

Risultato della ricerca: Otherpeer review


Inflammatory Bowel Diseases (IBD) is a chronic disorder characterized bya relapsing-remitting course, which alternates between active and quiescent states, ultimately impairing a patient's quality of life. The two main types of IBD are Crohn's disease (CD) and ulcerative colitis (UC). CD shows a transmural granulomatous inflammation that can involve any segment of the intestine affecting all layers of the intestinal wall while UC is limited to the mucosa and superficial sub-mucosa of the colon. In physiologial conditions the gut is costantly exposed to various antigens, commensal microflora and pathogens and the inflammatory response is finely balanced. Anyhow in some individuals with genetic susceptibility an anomalous inflammatory response can arise due to the deregulation of the negative feedback mechanisms implicated in its self-regulation. It is thought that a vast number of environmental risk factors may be implicated in the development of IBD, including smoking, dietary factors, psycological stress, use of non-steroidal anti-inflammatory drugs and oral contraceptive, appendectomy, breastfeeding, as el as infection. Nutritional support as a primary therapy has a crucial role in the management of patients with IBD since it can control the inflammatory process, treat malnutrition and its consequence, and avoid the use of immune-modulating drugs and their side effects. The gut microbiota is clearly manipulated by dietary components such as in n-3 PUFA and coniugated linoleic acid (CLA) which favorably reduce endotoxin load via shifts in the composition and metabolic activity of the microbial community. In particular, the beneficial effect of n-3 polynsatured fatty acids(PUFAs) and fermentable fiber, during the remission/quiescent phase of both CD and UC is highlighted. In fact, PUFAs are associated with a less grade of inflammation since they are metabolized to 3-series prostaglandins and thromboxanes and 5-series leukotrienes and, in addition, exert antiinflammatory effects when compared with their n-6 PUFA counterparts. In similar action to dietary n-3 PUFA, coniugated linoleic acid (CLA) have been reported to ameliorate intestinal inflammation in animal models of IBD. In contrast to corticosteroids, CLA suppresses gut inflammatory response while echancing antigen specific responsiveness of T cells against viral and bacterial pathogens. Avaitable data about nutritional intervention do not always match due to the incomplete knowledge of pathogenic mechanism underly ing IBD development. Further studies are therefore needed to improve nutritional therapeutic approach. In particular, is still unclear the role of the fiber in helping the remission of the disease. There are mainly two theories. One one hand, dietary fibers casn act as effective prebiotic by altering the intestinal microbial composition and promoting the growth of beneficial bacterial comunities within the large intestine. Some authors reported a positive effect associated with the production by colonic microflora and short chasin fatty acids (SCFA), able to down-regulate the production of pro-inflammatory cytokines to promote the restoration of intracellular reactive Oxygen Specie (ROS) balance, and the activation of NFG-KB. On the other hand, fiber can promote diarrhea, pain and gas aggravating the clinical state. We suggest that the consumption of fermentable fibers may have a good impact on patien's health. Now I wel knownthat version that various SNPs are linked to the risk of IBD development and therefore there is the possibility of predict if an individual is pre
Lingua originaleEnglish
Numero di pagine1
Stato di pubblicazionePublished - 2015

All Science Journal Classification (ASJC) codes

  • ???subjectarea.asjc.1300.1300???
  • ???subjectarea.asjc.1100.1110???
  • ???subjectarea.asjc.2700.2704???


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