The Vaginal Microbiome–Mitochondria Axis: Implications for Genital Tract Infections
4 affiliations
- 1Unit of Obstetrics and Gynecology, Fondazione Poliambulanza Istituto Ospedaliero, 25124 Brescia, Italy
- 2Department of Surgical, Medical, Dental and Morphological Sciences with Interest in Transplant, Oncological and Regenerative Medicine, University of Modena and Reggio Emilia, 41124 Modena, Italy
- 3Department of Obstetrics and Gynecology, IRCCS San Raffaele Scientific Institute, 20132 Milan, Italy
- 4Sbarro Institute for Cancer Research and Molecular Medicine and Center of Biotechnology, College of Science and Technology, Temple University, Philadelphia, PA 19122, USA
Abstract
The vaginal microbiome influences epithelial and immune homeostasis through microbial metabolites, virulence factors, and other molecular signals, yet intracellular mechanisms translating microbial activity into host responses remain largely unexplored. Here, we propose the vaginal microbiome–mitochondria axis as a functional framework linking microbial activity to host-cell metabolism, redox signaling, immunity, and cell fate. We integrated evidence from vaginal microbiology, mitochondrial biology, mucosal immunology, and immunometabolism, distinguishing direct observations in the female genital tract from mechanistic evidence obtained in other host–microbe systems. Available evidence indicates that microbial products relevant to vaginal homeostasis and dysbiosis can modulate mitochondrial bioenergetics, reactive oxygen species generation and redox signaling, membrane potential, dynamics, and quality control pathways, while mitochondrial responses can influence epithelial integrity and antimicrobial and inflammatory functions. We further propose that the balance between mitochondrial adaptation and dysfunction may contribute to resolution or persistence of vaginal disorders and that incomplete mitochondrial recovery could contribute to an incomplete microbial ecosystem–host reset and recurrence. Although direct vaginal evidence remains limited, this framework identifies mitochondria as a potentially important functional interface between microbial ecology and host response and generates testable hypotheses for investigating whether mitochondrial homeostasis contributes to durable resolution of vaginal dysbiosis and infection.
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BibTeX
@article{agoni2026vaginal,
title = {{The Vaginal Microbiome–Mitochondria Axis: Implications for Genital Tract Infections}},
author = {Lorenzo Agoni and Eva Pericolini and Stefano Salvatore and Massimo Candiani and Francesco De Seta},
journal = {Cells},
year = {2026},
month = oct,
doi = {10.3390/cells15201835},
url = {https://www.mdpi.com/2073-4409/15/20/1835},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - The Vaginal Microbiome–Mitochondria Axis: Implications for Genital Tract Infections
AU - Lorenzo Agoni
AU - Eva Pericolini
AU - Stefano Salvatore
AU - Massimo Candiani
AU - Francesco De Seta
PY - 2026
DA - 2026/10/09
JO - Cells
DO - 10.3390/cells15201835
UR - https://www.mdpi.com/2073-4409/15/20/1835
AB - The vaginal microbiome influences epithelial and immune homeostasis through microbial metabolites, virulence factors, and other molecular signals, yet intracellular mechanisms translating microbial activity into host responses remain largely unexplored. Here, we propose the vaginal microbiome–mitochondria axis as a functional framework linking microbial activity to host-cell metabolism, redox signaling, immunity, and cell fate. We integrated evidence from vaginal microbiology, mitochondrial biology, mucosal immunology, and immunometabolism, distinguishing direct observations in the female genital tract from mechanistic evidence obtained in other host–microbe systems. Available evidence indicates that microbial products relevant to vaginal homeostasis and dysbiosis can modulate mitochondrial bioenergetics, reactive oxygen species generation and redox signaling, membrane potential, dynamics, and quality control pathways, while mitochondrial responses can influence epithelial integrity and antimicrobial and inflammatory functions. We further propose that the balance between mitochondrial adaptation and dysfunction may contribute to resolution or persistence of vaginal disorders and that incomplete mitochondrial recovery could contribute to an incomplete microbial ecosystem–host reset and recurrence. Although direct vaginal evidence remains limited, this framework identifies mitochondria as a potentially important functional interface between microbial ecology and host response and generates testable hypotheses for investigating whether mitochondrial homeostasis contributes to durable resolution of vaginal dysbiosis and infection.
SN - 2073-4409
ER -