Inflammatory bowel disease (IBD) is a complex, multi-factorial disease thought to arise from an inappropriate immune response to commensal bacteria in a genetically susceptible person that results in chronic, cyclical, intestinal inflammation. Dietary and environmental factors are implicated in the initiation and perpetuation of IBD; however, a singular causative agent has not been identified. As of now, the role of environmental priming or triggers in IBD onset and pathogenesis are not well understood, but these factors appear to synergize with other disease susceptibility factors. In previous work, we determined that the polysaccharide dietary additive, maltodextrin (MDX), impairs cellular anti-bacterial responses and suppresses intestinal anti-microbial defense mechanisms. In this addendum, we review potential mechanisms for dietary deregulation of intestinal homeostasis, postulate how dietary and genetic risk factors may combine to result in disease pathogenesis, and discuss these ideas in the context of recent findings related to dietary interventions for IBD.
Keywords: AIEC, adherent-invasive Escherichia coli; CD, Crohn's disease; CMC, carboxymethyl cellulose; Crohn's disease; DSS, dextran sulfate sodium; FDA, Food and Drug Administration; GRAS, Generally Recognized As Safe; IBD, inflammatory bowel disease; IBD-AID, inflammatory bowel disease-anti-inflammatory diet; MDX, maltodextrin; SCD, specific carbohydrate diet; UC, ulcerative colitis; anti-microbial defense; diet; dietary additive; inflammatory bowel disease; intestinal homeostasis; maltodextrin; mucosal defense.