Bacterial peptidoglycan given late in life extended lifespan in worms and mice
In this abstract, bacterial peptidoglycan (PGN) is reported to activate lysosomes via V-ATPase binding and to extend lifespan in C. elegans and mice; late-life PGN supplementation in mice is described as prolonging lifespan and improving healthspan. [1]
Automatic summary · not editorially reviewed
The key findings
Aging is reported to reduce intestinal lysozyme expression, impairing bacterial cell-wall digestion and causing systemic PGN deficiency. [1]
In mice, PGN supplementation starting at 18 months of age is reported to significantly prolong lifespan and improve healthspan. [1]
The longevity effect is described as abolished by V-ATPase inhibition or genetic disruption of lysosomal components. [1]
The source at a glance
- Study type / format
- Preclinical study reported in an abstract
- Population / context
- C. elegans and mice, including mice given PGN from 18 months of age
- Summary based on
- Study abstract
- Publication status
- Preprint · peer-review status not confirmed
- Original publication
- September 2, 2026
Aging, lysozyme decline and PGN in worms and mice
The abstract frames lysosomal dysfunction as a hallmark of aging and asks whether microbial components regulate this organelle to influence longevity. It reports that aging reduces intestinal lysozyme expression, impairing digestion of bacterial cell walls and causing a systemic PGN deficiency. PGN is described as an evolutionarily conserved activator of lysosomal function that extends lifespan in both C. elegans and mice. These are reported associations and experimental findings in the abstract, not evidence that PGN causes human lifespan benefits.
Supporting source [1]
Late-life PGN supplementation in mice and V-ATPase mechanism
In mice, PGN supplementation starting at 18 months of age is reported to significantly prolong lifespan and improve healthspan. Mechanistically, PGN is said to localize to lysosomes and directly bind V-ATPase subunits, enhancing ATP hydrolysis and promoting lysosomal acidification. The effect is described as abolished by V-ATPase inhibition with bafilomycin A1 or by genetic disruption of lysosomal components (cup-5 and vha-12 mutants). The abstract also reports that PGN restores lysosomal acidification in aged cells, alleviates cellular senescence markers and improves locomotion and muscle integrity.
Supporting source [1]
Abstract-only scope of the gut–lysosome–longevity claim
The authors conclude that hosts exploit bacterial cell wall components to maintain cellular homeostasis, describing a gut microbiome–lysosome–longevity axis with implications for microbiome-based anti-aging interventions. These are the authors' interpretations of preclinical work in worms and mice. The abstract does not report human data, sample sizes, follow-up details or effect sizes, and the full text was not reviewed. The proposed axis and intervention implications are therefore not established for humans.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. No human data, sample sizes, follow-up or effect sizes are reported. Findings in C. elegans and mice are preclinical and do not establish human lifespan benefits.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Fu H, Tie J, Zhou Y, Wang X, Shan Z, Qi B. · europepmc.org · September 2, 2026