AMELIORATION OF CHRONIC INFLAMMATION BY INGESTION OF ELEMENTAL DIET IN A RAT MODEL OF GRANULOMATOUS ENTERITIS

Citation
S. Tanaka et al., AMELIORATION OF CHRONIC INFLAMMATION BY INGESTION OF ELEMENTAL DIET IN A RAT MODEL OF GRANULOMATOUS ENTERITIS, Digestive diseases and sciences, 42(2), 1997, pp. 408-419
Citations number
39
Categorie Soggetti
Gastroenterology & Hepatology
ISSN journal
01632116
Volume
42
Issue
2
Year of publication
1997
Pages
408 - 419
Database
ISI
SICI code
0163-2116(1997)42:2<408:AOCIBI>2.0.ZU;2-S
Abstract
The beneficial effect of elemental diet (ED) in the treatment of Crohn 's disease is reported, although the exact mechanism for this remains to be elucidated. In this study the effects of ED on intestinal inflam mation were investigated in a rat model of granulomatous enteritis. In testinal inflammation was induced by a single intramural injection of peptidoglycan-polysaccharide (PG-PS) from group A streptococci into ra t ileal Peyer's patches. A single injection of PG-PS in combination wi th fibrinogen, which retains PG-PS at the injection site, induced seve re granulomatous inflammation associated with mucosal ulceration. Immu no-histochemical study and immunocytochemical analysis of the cell sus pension from Peyer's patches showed accumulation of macrophages and an increase in interleukin-2 receptor (IL-2R)-positive T cells after PG- PS treatment. Chemiluminescence (ChL) activity and nitrite and nitrate (NOx) levels in the mesenteric venous blood as well as Ca2+-independe nt (inducible) nitric oxide synthase (NOS) activity in Peyer's patches were increased by PG-PS treatment. In rats fed with ED, both macrosco pic and histologic damage scores were significantly decreased as compa red with those in rats fed with the control diet. ED inhibited the inc rease in the numbers of macrophages and IL-2R-positive T cells in Prye r's patches. Increased ChL activity, NOx levels, and Ca2+-independent NOS activity were also reduced significantly by feeding with ED. These data suggest that ED reduces progression of PG-PS-induced chronic int estinal inflammation by modulating activation of T cells, production o f nitric oxide, and generation of oxygen free radicals.