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Spleen development is modulated by neonatal gut microbiota
M Manuela Rosado1, Alaitz Aranburu1, Marco Scarsella1
1B Cell Physiopathology Unit, Immunology Research Area, Bambino Gesù Children Hospital, Rome, Italy.
Immunology Letters
|May 2, 2018
Summary
Maternal milk’s secretory IgA (SIgA) promotes gut microbiota diversity, crucial for spleen immune system development in newborns. Lack of SIgA impairs spleen follicle formation and T-dependent antigen responses.
Area of Science:
- Immunology
- Microbiology
- Developmental Biology
Background:
- Mammalian immune system development is post-natal, driven by antigen exposure.
- The gut microbiota is critical for immune homeostasis, balancing effector and tolerogenic responses.
- The impact of gut bacteria on spleen maturation remains largely unknown.
Purpose of the Study:
- To investigate how colonizing bacteria influence spleen maturation in newborns.
- To determine the role of milk secretory IgA (SIgA) in modulating neonatal gut microbiota and its downstream effects on the spleen.
Main Methods:
- Generated immunocompetent mice from IgA-proficient and IgA-deficient mothers.
- Analyzed neonatal gut microbiota composition and diversity.
- Assessed spleen immune cell populations, follicular structure, and T-dependent antigen responses.
Main Results:
- Maternal milk SIgA promotes gut microbiota diversity in neonates.
- Neonates lacking milk SIgA exhibit impaired spleen Follicular Dendritic Cell (FDC) network and primary follicle development.
- Absence of SIgA leads to compromised T-dependent antigen responses and altered spleen/gut plasma cell populations.
Conclusions:
- Neonatal exposure to milk SIgA is essential for proper spleen immune system development.
- SIgA-mediated modulation of gut microbiota diversity is critical for establishing robust adaptive immune responses.
- Disruption of the early gut-immune axis can have long-lasting consequences on immune competence.
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