The Dietary Polysaccharide Maltodextrin Promotes <i>Salmonella</i> Survival and Mucosal Colonization in Mice

<div><p>In the latter half of the 20^th century, societal and technological changes led to a shift in the composition of the American diet to include a greater proportion of processed, pre-packaged foods high in fat and carbohydrates, and low in dietary fiber (a “Western diet”). Over the same time period, there have been parallel increases in <i>Salmonella</i> gastroenteritis cases and a broad range of chronic inflammatory diseases associated with intestinal dysbiosis. Several polysaccharide food additives are linked to bacterially-driven intestinal inflammation and may contribute to the pathogenic effects of a Western diet. Therefore, we examined the effect of a ubiquitous polysaccharide food additive, maltodextrin (MDX), on clearance of the enteric pathogen <i>Salmonella</i> using both <i>in vitro</i> and <i>in vivo</i> infection models. When examined <i>in vitro</i>, murine bone marrow-derived macrophages exposed to MDX had altered vesicular trafficking, suppressed NAPDH oxidase expression, and reduced recruitment of NADPH oxidase to <i>Salmonella</i>-containing vesicles, which resulted in persistence of <i>Salmonella</i> in enlarged Rab7⁺ late endosomal vesicles. <i>In vivo</i>, mice consuming MDX-supplemented water had a breakdown of the anti-microbial mucous layer separating gut bacteria from the intestinal epithelium surface. Additionally, oral infection of these mice with <i>Salmonella</i> resulted in increased cecal bacterial loads and enrichment of lamina propria cells harboring large Rab7⁺ vesicles. These findings indicate that consumption of processed foods containing the polysaccharide MDX contributes to suppression of intestinal anti-microbial defense mechanisms and may be an environmental priming factor for the development of chronic inflammatory disease.</p>