HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Figures Only Full Text Full Text (PDF) Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Oz, H. S. Articles by McClain, C. J. Search for Related Content PubMed PubMed Citation Articles by Oz, H. S. Articles by McClain, C. J.

Efficacy of a Transforming Growth Factor ß2 Containing Nutritional Support Formula in a Murine Model of Inflammatory Bowel Disease

Department of Medicine, Section of Gastroenterology/Nutrition, Rush University Medical Center, Chicago, Illinois (H.S.O.), Louisville, Kentucky
Department of Pathology (M.R.), Louisville, Kentucky
Department of Pharmacology/Toxicology (T.S.C., C.J.M.), Louisville, Kentucky
University of Louisville Medical School, VAMC (C.J.M.), Louisville, Kentucky

Address reprint requests to: Helieh S. Oz, DVM, PhD, Assistant Professor of Medicine, Director, Animal Studies Program in Digestive Diseases, Department of Medicine, Section of Gastroenterology/Nutrition Rush University Medical Center, Suite 206, 1725 W Harrison, Chicago, IL 60612. E-mail: helieh_oz{at}rush.edu

Objective: Dietary, environmental and genetic events may influence host susceptibility to inflammatory bowel diseases (IBD). Transforming growth factor ß2 (TGF-ß2), a multifunctional polypeptide (cytokine) present in human and bovine milk, plays a critical role in the development of tolerance, the prevention of autoimmunity, and in anti-inflammatory responses. TGF-ß2 is a potent inhibitor of intestinal epithelial cell (IEC) growth and stimulates IEC differentiation. The objective of this study was to determine whether a diet containing TGF-ß2 modulates intestinal injury and immune responses in an Interleukin-10 knockout (IL-10–/–) mouse model of IBD.

Methods: Five-week-old IL-10–/– mice (in BALB/c background) reared in our transgenic facility were fed either an enteral diet (Diet-A) containing TGF-ß2 or a control enteral diet (Diet-B) not rich in TGF-ß2. Mice were weighed weekly, monitored for illness and euthanized after eight weeks on the diet.

Results: Final weights were 28 ± 1.2 g (58.2% gain) for Diet-A mice and 23 ± 1.6 g (32.9% gain) for Diet-B mice (p = 0.0194). The hematocrits were 48.3% for Diet-A compared to 42% for Diet-B mice (p = 0.0021). Mice on Diet-A had significantly lower serum TNF- concentrations. Forty-four percent of mice on Diet-B developed severe diarrhea and rectal prolapse compared with none on Diet-A. Evaluation of intestinal pathology (score 0–4) revealed that animals fed Diet-A had a score of 2.1 ± 0.4 compared to 3.2 ± 0.36 in the Diet-B group (p = 0.040). The acute phase protein, serum amyloid A (SAA), was 3.8 times higher in the Diet-B group (p = 0.0038).

Conclusions: IL-10–/– mice fed a TGF-ß2 containing diet gained more weight, did not develop diarrhea or prolapse, had lower pathological scores, and lower SAAs. These data further support the use of TGF-ß2 containing enteral diets as one mode of therapy for Crohn’s disease.

Key words: IBD, Crohn’s disease, TGF-ß2, enterocolitis

This article has been cited by other articles:

				D. M. Wiese, R. Rivera, and D. L. Seidner Is There a Role for Bowel Rest in Nutrition Management of Crohn's Disease? Nutr Clin Pract, June 1, 2008; 23(3): 309 - 317. [Abstract] [Full Text] [PDF]

				T. T. MacDonald, A. DiSabatino, and J. N. Gordon Immunopathogenesis of Crohn's Disease JPEN J Parenter Enteral Nutr, July 1, 2005; 29(4_suppl): S118 - S125. [Abstract] [Full Text] [PDF]