Extracellular vesicles isolated from milk can improve gut barrier dysfunction induced by malnutrition
| Autor: | Robert H. J. Bandsma, Agostino Pierro, Abderrahim Benmoussa, Mohamed Karim Maghraby, Celine Bourdon, Andrea C Postmus, Abdirahman I. Abdi, Catriona Ling, Lijun Chi, Bo Li, Patrick Provost |
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| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: |
Male
medicine.medical_specialty Low protein Mouse medicine.medical_treatment Science Severe Acute Malnutrition Article 03 medical and health sciences chemistry.chemical_compound Extracellular Vesicles Mice 0302 clinical medicine Atrophy Low-protein diet Intestinal mucosa Internal medicine medicine Animals Gastrointestinal models Intestinal Mucosa Fluorescein isothiocyanate 030304 developmental biology 2. Zero hunger 0303 health sciences Multidisciplinary Intestinal permeability business.industry Intestinal villus Intestinal stem cells Malnutrition Epithelial Cells medicine.disease 3. Good health Diet Mice Inbred C57BL Disease Models Animal medicine.anatomical_structure Endocrinology Milk chemistry 030220 oncology & carcinogenesis Medicine Female business Diet Therapy |
| Zdroj: | Scientific Reports, Vol 11, Iss 1, Pp 1-14 (2021) Scientific Reports Scientific Reports, 11:7635. Nature Publishing Group |
| ISSN: | 2045-2322 |
| DOI: | 10.1038/s41598-021-86920-w |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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