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在重度急性营养不良的生理小鼠模型中，营养干预下的长期生态失调与免疫改变。

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

作者信息

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

机构信息

Aix Marseille University, CNRS, INSERM, CIML, Turing Centre for Living Systems, Marseille, France.

Escuela de Microbiología, Facultad de Ciencias, Universidad Nacional Autónoma de Honduras, Tegucigalpa, Honduras.

出版信息

iScience. 2023 May 19;26(6):106910. doi: 10.1016/j.isci.2023.106910. eCollection 2023 Jun 16.

DOI:10.1016/j.isci.2023.106910
PMID:37378323
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10291336/
Abstract

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.

摘要

重度急性营养不良（SAM）是一种影响全球数百万儿童的多因素疾病。它与肠道生理、微生物群和黏膜免疫的变化有关，这凸显了开展多学科研究以阐明其完整发病机制的必要性。我们建立了一个实验模型，用断奶小鼠喂养高度缺乏营养的饮食，模拟儿童SAM的关键人体测量学和生理学特征。这种饮食会改变肠道微生物群（分节丝状菌减少、与上皮细胞的空间距离）、新陈代谢（丁酸盐减少）以及免疫细胞群体（派尔集合淋巴结中的溶菌性树突状细胞和肠道Th17细胞耗竭）。营养干预可使动物测量学和肠道生理学快速恢复，但肠道微生物群、新陈代谢和免疫系统无法完全恢复。总之，我们提供了一个SAM的临床前模型，并确定了在免疫系统发育过程中进行未来干预以改善SAM整体缺陷的关键靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/54db/10291336/2b629a718ba5/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/54db/10291336/12158cd4abd5/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/54db/10291336/674e07038c82/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/54db/10291336/285c3374e9b0/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/54db/10291336/873e94c4ac63/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/54db/10291336/443d7e9895d6/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/54db/10291336/833516eeb450/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/54db/10291336/a0b8719ff945/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/54db/10291336/2b629a718ba5/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/54db/10291336/12158cd4abd5/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/54db/10291336/674e07038c82/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/54db/10291336/285c3374e9b0/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/54db/10291336/873e94c4ac63/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/54db/10291336/443d7e9895d6/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/54db/10291336/833516eeb450/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/54db/10291336/a0b8719ff945/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/54db/10291336/2b629a718ba5/gr7.jpg

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

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[1]
Investigating the Role of Gut Microbiota in the Pathogenesis and Progression of Rheumatoid Arthritis in a Collagen-Induced Arthritis Mouse Model.

Int J Mol Sci. 2025-5-26

[2]
Substitution of polysorbates by plant-based emulsifiers: impact on vitamin D bioavailability and gut health in mice.

Commun Biol. 2025-6-7

[3]
Protective effects of Lactobacillus plantarum strain against protein malnutrition-induced muscle atrophy and bone loss in juvenile mice.

PLoS One. 2025-1-16

[4]
Gut microbiota and childhood malnutrition: Understanding the link and exploring therapeutic interventions.

Eng Life Sci. 2023-10-5

本文引用的文献

[1]
Microbe-mediated intestinal NOD2 stimulation improves linear growth of undernourished infant mice.

Science. 2023-2-24

[2]
Vitamin D alleviates non-alcoholic fatty liver disease restoring gut microbiota and metabolism.

Front Microbiol. 2023-2-2

[3]
The role of the tryptophan-NAD + pathway in a mouse model of severe malnutrition induced liver dysfunction.

Nat Commun. 2022-12-8

[4]
Stunted children display ectopic small intestinal colonization by oral bacteria, which cause lipid malabsorption in experimental models.

Proc Natl Acad Sci U S A. 2022-10-11

[5]
Microbiota imbalance induced by dietary sugar disrupts immune-mediated protection from metabolic syndrome.

Cell. 2022-9-15

[6]
Akkermansia muciniphila: paradigm for next-generation beneficial microorganisms.

Nat Rev Gastroenterol Hepatol. 2022-10

[7]
Cross-feeding between intestinal pathobionts promotes their overgrowth during undernutrition.

Nat Commun. 2021-11-25

[8]
Environmental enteric dysfunction induces regulatory T cells that inhibit local CD4+ T cell responses and impair oral vaccine efficacy.

Immunity. 2021-8-10

[9]
Spatial and temporal key steps in early-life intestinal immune system development and education.

FEBS J. 2022-8

[10]
The Keystone commensal bacterium Christensenella minuta DSM 22607 displays anti-inflammatory properties both in vitro and in vivo.

Sci Rep. 2021-6-1

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