Abstract
Prebiotic oligosaccharides are used to modulate enteric pathogens and reduce pathogen shedding. The interactions with prebiotics that alter Listeria monocytogenes infection are not yet clearly delineated. L. monocytogenes cellular invasion requires a concerted manipulation of host epithelial cell membrane receptors to initiate internalization and infection often via receptor glycosylation. Bacterial interactions with host glycans are intimately involved in modulating cellular responses through signaling cascades at the membrane and in intracellular compartments. Characterizing the mechanisms underpinning these modulations is essential for predictive use of dietary prebiotics to diminish pathogen association. We demonstrated that human milk oligosaccharide (HMO) pretreatment of colonic epithelial cells (Caco-2) led to a 50% decrease in Listeria association, while Biomos pretreatment increased host association by 150%. L. monocytogenes-induced gene expression changes due to oligosaccharide pretreatment revealed global alterations in host signaling pathways that resulted in differential subcellular localization of L. monocytogenes during early infection. Ultimately, HMO pretreatment led to bacterial clearance in Caco-2 cells via induction of the unfolded protein response and eIF2 signaling, while Biomos pretreatment resulted in the induction of host autophagy and L. monocytogenes vacuolar escape earlier in the infection progression. This study demonstrates the capacity of prebiotic oligosaccharides to minimize infection through induction of host-intrinsic protective responses.
Highlights
Listeria monocytogenes is an intracellular, foodborne, enteric pathogen that is pervasive in livestock, the food supply and the environment
Upon invasion of the intestinal epithelial cell layer, L. monocytogenes reside in an intracellular vacuole, followed by vacuolar escape where the organism spreads to neighboring cells parallel to the basal lateral membrane [3]
Monolayers with the mannanoligosaccharides and inulin resulted in a 150% increase in Listeria host decreased L. monocytogenes in vitro host association
Summary
Listeria monocytogenes is an intracellular, foodborne, enteric pathogen that is pervasive in livestock, the food supply and the environment. The most at risk populations include children, pregnant women and the elderly. Infection begins with febrile gastroenteritis followed by progression to septicemia, meningitis, or death in immunocompromised individuals and neonatal meningitis or loss of the fetus in pregnant women [1]. Among the major foodborne pathogen-related illnesses, listeriosis presents with the highest mortality rate of any foodborne pathogens [2]. Upon invasion of the intestinal epithelial cell layer, L. monocytogenes reside in an intracellular vacuole, followed by vacuolar escape where the organism spreads to neighboring cells parallel to the basal lateral membrane [3]. Infection leads to cell death via apoptosis [4,5]
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