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
Categorie Soggetti
Gastroenterology & Hepatology
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.