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Updated: Jan 25, 2026
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Investigating Alterations in Caecum Microbiota After Traumatic Brain Injury in Mice
Published on: September 19, 2019
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Microbiota from young mice restore the function of aged ISCs
Kodandaramireddy Nalapareddy1, David B Haslam2, Ann-Kathrin Kissmann3
1Division of Experimental Hematology and Cancer Biology, Cincinnati Children's Hospital Medical Center and University of Cincinnati, Cincinnati, OH 45229, USA.
Stem Cell Reports
|January 23, 2026
Summary
Aging alters gut microbiota, reducing intestinal stem cell (ISC) function and regeneration. Specific bacteria like Akkermansia muciniphila exacerbate this decline by inhibiting Wnt signaling, suggesting microbiota modulation as a therapeutic strategy.
Area of Science:
- Gastroenterology
- Microbiology
- Cell Biology
Background:
- Intestinal homeostasis relies on intestinal stem cells (ISCs).
- Aging impairs ISC function and intestinal regeneration, linked to declining Wnt signaling.
- Gut microbiota composition shifts significantly with age.
Purpose of the Study:
- To investigate how aging-associated changes in gut microbiota affect ISC function and intestinal regeneration.
- To elucidate the role of specific microbial species, such as Akkermansia muciniphila, in regulating ISC activity.
Main Methods:
- Analysis of aging-associated changes in gut microbiota composition.
- In vivo studies using microbiota transfer experiments.
- Assessment of canonical Wnt signaling pathways and Ascl2 expression in ISCs.
Main Results:
- Aging-associated microbiota alterations reduce canonical Wnt signaling via Ascl2 in ISCs, impairing regenerative potential.
- Elevated Akkermansia muciniphila levels were found to inhibit Ascl2-mediated Wnt signaling, leading to reduced epithelial regeneration.
- Gut microbiota composition critically regulates ISC function.
Conclusions:
- Gut microbiota composition plays a crucial role in maintaining ISC function and intestinal regeneration during aging.
- Modulating the gut microbiota presents a potential therapeutic avenue for age-related decline in intestinal stem cell function.
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