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Updated: Aug 5, 2026
06:51
Techniques to Induce and Quantify Cellular Senescence
Published on: May 1, 2017
Host-Pathogen Interaction as a Driver of Cellular Senescence: Microbial Triggers and Host Response
Florin Iordache1, Alexandru Andrei Zaharie1, Petronela Mihaela Rosu1
1Faculty of Veterinary Medicine, University of Agronomic Sciences and Veterinary Medicine of Bucharest, Splaiul Independentei 105, 050097 Bucharest, Romania.
International Journal of Molecular Sciences
|July 28, 2026
Summary
Bacterial infections can accelerate cellular aging (senescence) and weaken the immune system (immunosenescence). This review explores how pathogens induce senescence, promoting inflammation and age-related diseases.
Area of Science:
- Immunology
- Cell Biology
- Microbiology
Background:
- Cellular senescence, aging, and host-pathogen interactions are complex and not fully understood.
- Bacterial infections are increasingly recognized as significant contributors to immunosenescence.
Purpose of the Study:
- To review cellular and molecular changes in senescent cells.
- To examine the role of bacterial infections in driving immunosenescence.
- To integrate knowledge on how bacterial pathogens induce senescence and impact host tissues.
Main Methods:
- Literature review focusing on cellular senescence, aging, and bacterial infections.
- Analysis of molecular mechanisms of pathogen-induced senescence.
- Examination of bacterial virulence factors' impact on host signaling pathways.
Main Results:
- Bacterial pathogens induce senescence through genotoxicity, oxidative stress, and signaling pathway disruption.
- Bacterial virulence factors modulate key pathways (e.g., p53-p21, NF-κB, mTOR, cGAS-STING).
- This modulation promotes a pro-inflammatory senescence-associated secretory phenotype (SASP), chronic infection, and tissue damage.
Conclusions:
- Bacterial infections contribute to premature aging and age-related diseases by inducing cellular senescence.
- Understanding these mechanisms offers novel therapeutic targets for modulating senescence and enhancing host resilience.
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