Imprinting of the immune system by the microbiota early in life
Open accessAbstract
The ontogeny and maturation of the immune system is modulated by the microbiota. During fetal life, the mother's microbiota produces compounds that are transferred to the fetus and offspring, and enhance the generation of innate immune cells. After birth, the colonizing microbiota induces the development of intestinal lymphoid tissues and maturation of myeloid and lymphoid cells, and imprints the immune system with a reactivity level that persists long after weaning into adulthood. When the cross-talk between host and microbiota is perturbed early in life, a pathological imprinting may develop that is characterized by excessive immune reactivity in adulthood, which translates into increased susceptibility to inflammatory pathologies. In this review, we discuss the recent data that demonstrate the existence of a time window of opportunity early in life during which mice and human have to be exposed to microbiota in order to develop a balanced immune system. We also discuss the factors involved in imprinting, such as the microbiota, immune cells and stromal cells, as well as the nature of imprinting.
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In the cross-talk between mucosal immunity and gut microbes, there are defined periods of plasticity, such as during weaning and neonatal periods when host lymphocytes and gut bacteria expand and colonize the intestinal mucosa.
“In the cross-talk between mucosal immunity and gut microbes, there are defined periods of plasticity, such as during weaning and neonatal periods when host lymphocytes and gut bacteria expand and colonize the intestinal mucosa. 80”
From Key determinants of success in fecal microbiota transplantation: From microbiome to clinic (2023) · cites this paper as [80]
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A Comparison Study of Age and Colorectal Cancer-Related Gut Bacteria
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The Adverse Effects of Prenatal METH Exposure on the Offspring: A Review
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Probiotics in Children with Asthma
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Microbiota Regulates Pancreatic Cancer Carcinogenesis through Altered Immune Response
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Amato, K. R., Pradhan, P. P., Mallott, E. K., Shirola, W., & Lu, A. (2024) · Evolution Medicine and Public Health · doi:10.1093/emph/eoae001 · Cited by 28 · see citing works
The impact of maternal exposure to antibiotics on the development of child gut microbiome
Miyoshi, J., & Hisamatsu, T. (2021) · Immunological Medicine · doi:10.1080/25785826.2021.1963189 · Cited by 24 · see citing works
Kiernan, D. P., O’Doherty, J. V., & Sweeney, T. (2023) · Animals · doi:10.3390/ani13192996 · Cited by 28 · see citing works
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Early‐Life Host–Microbial Interactions and Asthma Development: A Lifelong Impact?
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Delayed Gut Colonization Shapes Future Allergic Responses in a Murine Model of Atopic Dermatitis
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- Authors
- Al Nabhani, Z., & Eberl, G.
- Affiliations
- Inserm (FR)
- Corresponding author
- Eberl, Gérard
- ORCID
- Eberl, Gérard
- Venue
- Mucosal Immunology
- Publisher
- Elsevier BV
- Published
- 2020-03
- Volume
- 13
- Issue
- 2
- Pages
- 183-189
- ISSN
- 1933-0219 (ISSN-L)
- OpenAlex
- W3001781379
- Cited by
- 301
- References
- 90
- Citations by year
- 2026: 41 · 2025: 45 · 2024: 39 · 2023: 51 · 2022: 45 · 2021: 66 · 2020: 14
- FWCI
- 4.21
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Mucosal Immunology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Kenneth Rainin Foundation
- Institut National de la Santé et de la Recherche Médicale
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Life Sciences › Immunology and Microbiology › Immunology › Immune responses and vaccinations
- Keywords
- gut microbiota, early life, innate immune cells, intestinal lymphoid tissue, myeloid cell maturation, immunoreactivity, stromal cells, immune ontogeny
- MeSH terms
- Gastrointestinal Microbiome, Host Microbial Interactions, Adult, Animals, Female, Homeostasis, Humans, Immune System, Inflammation, Lymphocytes, Pregnancy, Mice
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