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Updated: Jul 30, 2025

Probiotic Studies in Neonatal Mice Using Gavage
Published on: January 27, 2019
Postnatal 14D is the Key Window for Mice Intestinal Development- An Insight from Age-Dependent Antibiotic-Mediated
Uday Pandey1,2, Subodh Tambat3, Palok Aich1,2
1School of Biological Sciences, National Institute of Science Education and Research (NISER), P.O. Jatni, Khurda, Odisha, 752050, India.
Insights
Antibiotic-induced gut microbiota disruption in neonatal mice significantly impairs intestinal barrier function and immune development, particularly at postnatal day 14. This highlights the critical role of specific gut bacteria in early life intestinal health.
Area of Science:
- Microbiology
- Immunology
- Developmental Biology
Background:
- The postnatal period is crucial for gastrointestinal tract and immune system development.
- Gut microbiota plays a vital role in host health, immunity, and development, but its early-life functions require further elucidation.
- Understanding gut microbiota's impact on intestinal integrity and immune profile during early development is essential.
Purpose of the Study:
- To investigate the effects of antibiotic-mediated gut microbiota perturbation on intestinal integrity, epithelial development, and immune profile in neonatal mice.
- To identify critical developmental periods and specific microbial compositions influencing neonatal intestinal health.
Main Methods:
- Antibiotic-induced gut microbiota perturbation in mice at postnatal days 7, 14, 21, and 28.
- 16S rRNA metagenomic analysis to assess microbial composition.
- Analysis of barrier integrity, tight junction proteins (TJPs), intestinal epithelial cell (IEC) markers, and inflammatory cytokines.
- Microbiota transplantation to confirm causal roles.
Main Results:
- Antibiotic treatment led to age-related changes in gut microbiota, increasing Proteobacteria and decreasing Bacteroidetes and Firmicutes.
- Significant disruption of intestinal barrier integrity, reduced TJPs and IEC markers, and increased systemic inflammation were observed at postnatal day 14.
- Microbiota transplantation demonstrated a causal role of specific bacteria in restoring barrier function.
Conclusions:
- Postnatal day 14 represents a critical window for neonatal intestinal development, significantly influenced by gut microbiota composition.
- Early-life gut microbiota perturbation can lead to detrimental effects on intestinal integrity and immune homeostasis.
- Specific microbial compositions are crucial for maintaining neonatal intestinal barrier functions.
Abstract:
The postnatal period is one of the critical windows for the structure-function development of the gastrointestinal tract and associated mucosal immunity. Along with other constituent members, recent studies suggest the contribution of gut microbiota in maintaining host health, immunity, and development. Although the gut microbiota's role in maintaining barrier integrity is known, its function in early life development still needs to be better understood. To understand the details of gut microbiota's effects on intestinal integrity, epithelium development, and immune profile, the route of antibiotic-mediated perturbation is taken. Mice on days 7(P7D), 14(P14D), 21(P21D) and 28(P28D) are sacrificed and 16S rRNA metagenomic analysis is performed. The barrier integrity, tight junction proteins (TJPs) expression, intestinal epithelial cell (IEC) markers, and inflammatory cytokines are analyzed. Results reveal a postnatal age-related impact of gut microbiota perturbation, with a gradual increase in the relative abundance of Proteobacteria and a reduction in Bacteroidetes and Firmicutes. Significant barrier integrity disruption, reduced TJPs and IECs marker expression, and increased systemic inflammation at P14D of AVNM-treated mice are found. Moreover, the microbiota transplantation shows recolonization of Verrucomicrobia, proving a causal role in barrier functions. The investigation reveals P14D as a critical period for neonatal intestinal development, regulated by specific microbiota composition.

