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Prolonged dysbiosis and altered immunity under nutritional intervention in a physiological mouse model of severe acute malnutrition

Severe acute malnutrition (SAM) is a multifactorial disease affecting millions of children worldwide. It is associated with changes in intestinal physiology, microbiota, and mucosal immunity, emphasizing the need for multidisciplinary studies to unravel its full pathogenesis. We established an exper...

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Detalles Bibliográficos
Autores principales: Hidalgo-Villeda, Fanny, Million, Matthieu, Defoort, Catherine, Vannier, Thomas, Svilar, Ljubica, Lagier, Margaux, Wagner, Camille, Arroyo-Portilla, Cynthia, Chasson, Lionel, Luciani, Cécilia, Bossi, Vincent, Gorvel, Jean-Pierre, Lelouard, Hugues, Tomas, Julie
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10291336/
https://www.ncbi.nlm.nih.gov/pubmed/37378323
http://dx.doi.org/10.1016/j.isci.2023.106910
Descripción
Sumario:Severe acute malnutrition (SAM) is a multifactorial disease affecting millions of children worldwide. It is associated with changes in intestinal physiology, microbiota, and mucosal immunity, emphasizing the need for multidisciplinary studies to unravel its full pathogenesis. We established an experimental model in which weanling mice fed a high-deficiency diet mimic key anthropometric and physiological features of SAM in children. This diet alters the intestinal microbiota (less segmented filamentous bacteria, spatial proximity to epithelium), metabolism (decreased butyrate), and immune cell populations (depletion of LysoDC in Peyer’s patches and intestinal Th17 cells). A nutritional intervention leads to a fast zoometric and intestinal physiology recovery but to an incomplete restoration of the intestinal microbiota, metabolism, and immune system. Altogether, we provide a preclinical model of SAM and have identified key markers to target with future interventions during the education of the immune system to improve SAM whole defects.