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Updated: May 16, 2025

Probiotic Studies in Neonatal Mice Using Gavage
Published on: January 27, 2019
Bifidobacteria support optimal infant vaccine responses.
Feargal J Ryan1,2, Michelle Clarke3,4,5, Miriam A Lynn1,2
1Precision Medicine, South Australian Health and Medical Research Institute (SAHMRI), Adelaide, South Australia, Australia.
Neonatal antibiotic exposure impairs infant vaccine responses by altering the gut microbiota. Restoring Bifidobacterium species in mice improved vaccine immunity, suggesting microbiota-targeted interventions could be beneficial.
Area of Science:
- Immunology
- Microbiology
- Neonatal Health
Background:
- Antibiotic exposure in early life is linked to reduced vaccine effectiveness.
- The underlying mechanisms for this impaired immune response are not well understood.
Purpose of the Study:
- To investigate the impact of early-life antibiotic exposure on infant immune responses to vaccination.
- To explore the role of the gut microbiota in mediating these effects.
Main Methods:
- Prospective follow-up of 191 infants from birth to 15 months.
- Systems vaccinology approach, including antibody titrations and transcriptional profiling.
- Faecal metagenomics to analyze gut microbiota composition.
Main Results:
- Neonatal antibiotic exposure, but not intrapartum exposure, was associated with lower antibody titres to pneumococcal and Hib/diphtheria antigens at 7 months.
- Infants exposed to neonatal antibiotics showed an inflammatory transcriptional profile before vaccination and reduced Bifidobacterium abundance.
- Reduced Bifidobacterium abundance correlated with lower vaccine antibody titres six months later.
- Preclinical models showed microbiota-dependent vaccine responses, restorable with Bifidobacterium species.
Conclusions:
- Early-life antibiotic exposure negatively impacts vaccine immunogenicity through microbiota alterations.
- Targeting the microbiota, for example with Bifidobacterium species, may restore vaccine responses.
- Microbiota-targeted interventions show promise for mitigating antibiotic-induced impairment of vaccine responses.
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