Inflammatory Bowel Diseases - ulcerative colitis and Crohn's disease- are chronic gastrointestinal inflammatory diseases of unknown etiology. Decreased oral intake, malabsorption, accelerated nutrient losses, increased requirements, and drug-nutrient interactions cause nutritional and functional deficiencies that require proper correction by nutritional therapy. The goals of the different forms of nutritional therapy are to correct nutritional disturbances and to modulate inflammatory response, thus influencing disease activity. Total parenteral nutrition has been used to correct and to prevent nutritional disturbances and to promote bowel rest during active disease, mainly in cases of digestive fistulae with high output. Its use should be reserved for patients who cannot tolerate enteral nutrition. Enteral nutrition is effective in inducing clinical remission in adults and promoting growth in children. Due to its low complication rate and lower costs, enteral nutrition should be preferred over total parenteral nutrition whenever possible. Both present equal effectiveness in primary therapy for remission of active Crohn's disease. Nutritional intervention may improve outcome in certain individuals; however, because of the costs and complications of such therapy, careful selection is warranted, especially in patients presumed to need total parenteral nutrition. Recent research has focused on the use of nutrients as primary treatment agents. Immunonutrition is an important therapeutic alternative in the management of inflammatory bowel diseases, modulating the inflammation and changing the eicosanoid synthesis profile. However, beneficial reported effects have yet to be translated into the clinical practice. The real efficacy of these and other nutrients (glutamine, short-chain fatty acids, antioxidants) still need further evaluation through prospective and randomized trials.

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Although graft-versus-host disease (GVHD) has been a major concern after small-bowel transplantation (SBTX), the lack of suitable experimental model has allowed only limited study of GVHD after solid-organ transplantation. 1 We recently developed a clinically relevant experimental animal model of GVHD of fully allogeneic SBTX. This study describes histopathological evolution of the disease, cytokine involvement, responsible donor cells, and preliminary results of treatment using recipient and third-party cell infusion. MATERIALS AND METHODSLewis (LEW, RT11) rat recipients received orthotopic SBTX and simultaneous donor bone marrow cell infusion (BMC, 250 × 10 6 ) from ACI (RT1 a ) rats. Tacrolimus (FK 506, 1 mg/kg per day) was administered on days 0 to 13, then continued as a weekly injection of same dose for 350 days. The number of donor cells in the recipient circulation was determined by flow cytometry using antibodies specific for donor and recipient MHC class I (MAbs MN4-91-6 and 163). Reverse-transcription polymerase chain reaction (RT-PCR) using 32 P-labeled primers was used to measure the levels of cytokine mRNA in the graft and recipient tissues. RESULTSDonor cells persisted in the recipients for more than 300 days after transplantation and accounted for 5% to 25% of lymphocytes in the circulation. The gradual increase of donor cells in these animals correlated with the appearance of clinical signs of GVHD (skin rash, hyperkeratosis, body weight, and hair loss) with a median onset of 104 days (range 98 to 114 days). These signs of GVHD waxed and waned for the rest of the experimental period, and eventually all animals died of GVHD or other transplantation-related complication, such as infection, with a median survival of 244 days. Cytokine analysis revealed the association of the histopathological changes of GVHD (grades I-III) and the upregulation of IFN-γ, TNF-α, IL-6, and IL-10 in the cervical lymph nodes and skin before and after animals showing clinical signs of GVHD. However, donor and recipient small bowel in this model did not show any increased expression of cytokine mRNA or histopathological changes.Efficacy of immunomodulatory treatment of GVHD was examined using this GVHD model of SBTX and BMC. In vivo ACI (donor strain)-primed splenocytes were prepared from LEW (recipient strain) or PVG (third-party strain) rats that received simultaneous ACI heart

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