Synbiotic promotion of epithelial proliferation by orally ingested encapsulated Bifidobacterium breve and raffinose in the small intestine of rats

Abstract

We evaluated the effects of Bifidobacterium breve JCM1192(T )and/or raffinose on epithelial proliferation in the rat small and large intestines. WKAH/Hkm Slc rats (4 wk old) were fed a control diet, a diet supplemented with either encapsulated B. breve (30 g/kg diet, 1.5 x 10(7) colony-forming unit/g capsule) or raffinose (30 g/kg diet), or a diet supplemented with both encapsulated B. breve and raffinose, for 3 wk. Epithelial proliferation in the small intestine, as assessed by bromodeoxyuridine immunohistochemistry, was increased only in the B. breve plus raffinose-fed group. We determined the number of bifidobacteria in cecal contents using fluorescence in situ hybridization and confirmed the presence of ingested B. breve only in the B. breve plus raffinose-fed group. This suggests that the ingested B. breve cells used raffinose and were activated in the small intestine, where they subsequently influenced epithelial proliferation. In conclusion, we found a prominent synbiotic effect of encapsulated B. breve in combination with raffinose on epithelial proliferation in rat small intestine but not in large intestine. To our knowledge, this is the first report of a synbiotic that affects epithelial proliferation.

Host-derived glycans serve as selected nutrients for the gut microbe: human milk oligosaccharides and bifidobacteria†

“…The presence of bifidobacteria in the gut microbiota appears to be correlated with a reduced incidence of diseases such as diarrhea and allergies in infants. 17) Various beneficial effects of bifidobacteria on host health have been reported, including the inhibition of harmful bacteria, 17) fortification of barrier function of intestinal epithelial cells, 18) and modulation of immune function. 19) Thus, the bacteria might be the first evolutionary commensals in the human gut, but the molecular mechanism underlying the formation of bifidobacteria-rich microbiota in the intestines of breast-fed infants remains elusive.…”

An ATP Binding Cassette Transporter Mediates the Uptake of α-(1,6)-Linked Dietary Oligosaccharides in Bifidobacterium and Correlates with Competitive Growth on These Substrates

“…Similarly, isomalto-oligosaccharides (IMOs), comprising ␣-(1,6)-gluco-oligosaccharides derived from breakdown of starch and the bacterial exopolysaccharide dextran (13,14), are resistant to degradation by human digestive enzymes. Both of these classes of ␣-(1,6)-oligosaccharides selectively boost the counts of bifidobacteria and gut-adapted lactobacilli in vitro and in vivo (10,15), but the molecular basis of this preferential enumeration is unclear.…”

Raffinose family oligosaccharide utilisation by probiotic bacteria: insight into substrate recognition, molecular architecture and diversity of GH36 α-galactosidases

“…The growth of several probiotic lactobacilli and bifidobacteria on RFO is well documented (Dinoto et al 2006;Ishizuka et al 2009;Su et al 2007), and raffi nose utilisation loci have been described in some lactobacilli (Carrera-Silva et al 2006;Silvestroni et al 2002). In recent years, however, the availability of a large number of genome sequences revealed remarkable diversity in the genetic organisation of RFO utilisation.…”

“…This is particularly interesting as RFOs, which are abundant in many foods, are not digestible in monogastric animals and thus are able to reach the colon intact, thereby stimulating the growth of gut microbiota. Historically, RFOs have been considered as anti-nutritional factors, but this view is being revised as ingestion of RFO in the right dose did not seem to cause discomfort, but was shown to stimulate the growth of benefi cial gut microbes and suppress the growth of pathogens suggesting a prebiotic effect (Dinoto et al 2006;Ishizuka et al 2009;Martinez-Villaluenga et al 2008;Su et al 2007).…”