We investigated the effect of resistant maltodextrin (RMD), a non-viscous soluble dietary fiber, on
intestinal immune response and its mechanism in mice. Intestinal and fecal immunoglobulin A (IgA) were
determined as indicators of intestinal immune response, and changes in the intestinal environment were focused
to study the mechanism. BALB/c mice were fed one of three experimental diets, a control diet or a diet
containing either 5% or 7.5% RMD, for two weeks. Continuous intake of RMD dose-dependently increased total IgA
levels in the intestinal tract. Total IgA production from the cecal mucosa was significantly increased by RMD
intake, while there were no significant differences in mucosal IgA production between the control group and
experimental groups in the small intestine and colon. Continuous intake of RMD changed the composition of the
cecal contents; that is, the composition of the cecal microbiota was changed, and short-chain fatty acids
(SCFAs) were increased. There was an increased trend in Bacteroidales in the cecal microbiota, and butyrate,
an SCFA, was significantly increased. Our study demonstrated that continuous intake of RMD enhanced the
intestinal immune response by increasing the production of IgA in the intestinal tract. It suggested that the
increase in total SCFAs and changes in the intestinal microbiota resulting from the fermentation of RMD orally
ingested were associated with the induction of IgA production in intestinal immune cells, with the IgA
production of the cecal mucosa in particular being significantly increased.