The anti-inflammatory mechanism of
prebiotics has recently been shown to have an impact on the host immune system. DHNA from Propionibacterium freudenreichii is known to promote the proliferation of Bifidobacterium and can ameliorate
colitis, although its mode of action remains unknown. In this study, we investigated whether DHNA attenuates
inflammation in
piroxicam-treated IL-10(-/-) mice, particularly focusing on the changes of the host immune mechanism. DHNA was administered to IL-10(-/-) mice with
colitis, and the expression of adhesion molecules and
mRNA levels of proinflammatory
cytokines were determined. DHNA pretreatment attenuated the
piroxicam-induced histological changes. The increased F4/80-positive cell infiltration and
VCAM-1 expression were decreased by DHNA administration. The increased
mRNA levels of proinflammatory
cytokines were also suppressed by DHNA. In in vitro experiments, increased
mRNA levels of proinflammatory
cytokines after
endotoxin exposure were decreased significantly by DHNA pretreatment in RAW264.7, a macrophage cell line, and IL-10(-/-) mice BMMs, whereas the expression of
VCAM-1 in bEnd.3 cells, a endothelial cell line, was not affected. Taken together, these findings suggest that administration of DHNA is useful for the treatment of
colitis in
piroxicam-treated IL-10(-/-) mice and that attenuation of
colitis by DHNA may partly be a result of its direct action on intestinal macrophages to inhibit proinflammatory
cytokine production.