Abstract
Malnutrition impacts approximately 50 million children worldwide and is linked to 45% of global mortality in children below the age of five. Severe acute malnutrition (SAM) is associated with intestinal barrier breakdown and epithelial atrophy. Extracellular vesicles including exosomes (EVs; 30–150 nm) can travel to distant target cells through biofluids including milk. Since milk-derived EVs are known to induce intestinal stem cell proliferation, this study aimed to examine their potential efficacy in improving malnutrition-induced atrophy of intestinal mucosa and barrier dysfunction. Mice were fed either a control (18%) or a low protein (1%) diet for 14 days to induce malnutrition. From day 10 to 14, they received either bovine milk EVs or control gavage and were sacrificed on day 15, 4 h after a Fluorescein Isothiocyanate (FITC) dose. Tissue and blood were collected for histological and epithelial barrier function analyses. Mice fed low protein diet developed intestinal villus atrophy and barrier dysfunction. Despite continued low protein diet feeding, milk EV treatment improved intestinal permeability, intestinal architecture and cellular proliferation. Our results suggest that EVs enriched from milk should be further explored as a valuable adjuvant therapy to standard clinical management of malnourished children with high risk of morbidity and mortality.
Highlights
Malnutrition impacts approximately 50 million children worldwide and is linked to 45% of global mortality in children below the age of five
Body changes in milk extracellular vesicles (EVs)‐ and sham‐treated malnourished mice
Our study aimed to assess the effect of milk EVs on intestinal epithelial atrophy and barrier dysfunction in a mouse model of severe malnutrition
Summary
Malnutrition impacts approximately 50 million children worldwide and is linked to 45% of global mortality in children below the age of five. Since milk-derived EVs are known to induce intestinal stem cell proliferation, this study aimed to examine their potential efficacy in improving malnutrition-induced atrophy of intestinal mucosa and barrier dysfunction. Infections are common in children with complicated SAM and are related to immune impairments and the lack of ability to maintain an effective intestinal barrier that could lead to bacterial translocation across the intestinal lumen and subsequent sepsis[7,8,9]. To this date, there are no effective treatment modalities targeting the repair of the intestinal epithelial barrier function in malnourished children. In premature rat pups exposed to NEC inducing conditions, the administration of EVs significantly reduced disease severity[19,20,21,22]
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