Transcriptomic reprogramming and displacement of mastitis-associated Staphylococcus aureus biofilms by lactic acid bacteria
4 affiliations
- 1Dept. Galenic Pharmacy and Food Technology, Complutense University of Madrid, Madrid, Spain
- 2Centre of Biological Engineering (CEB), Laboratory of Research in Biofilms Rosário Oliveira (LIBRO), University of Minho, Braga, Portugal
- 3Multidisciplinary Institute, Complutense University of Madrid, Madrid, Spain
- 4Dept. Nutrition and Food Science, Complutense University of Madrid, Madrid, Spain
Abstract
Staphylococcus aureus is one of the main etiological agents of acute mastitis during lactation, and its ability to persist in biofilms can compromise conventional antimicrobial treatments. Lactic acid bacteria (LAB) have emerged as promising probiotic candidates for mastitis management, but the molecular mechanisms underlying their interaction with S. aureus remain poorly understood. This study aimed to evaluate the ability of three LAB strains (Limosilactobacillus fermentum I7, Limosilactobacillus reuteri 7SNG3–30 and Ligilactobacillus salivarius 22SNG3-30) to interfere with mature biofilms formed by two mastitis-associated S. aureus strains, SA4 and SA55, and to characterize the associated transcriptional responses. The LAB strains were able to colonize preformed 24-h S. aureus biofilms, eventually dominating the mixed-species communities and reducing the attached staphylococcal population. RT-qPCR showed limited transcriptional changes after 4 h of LAB exposure, followed by a broader 16-h response characterized by induction of the stress/adaptation marker uspA and repression of genes related to quorum sensing, virulence, biofilm matrix production and iron acquisition. RNA-seq analysis of SA4 biofilms exposed to LAB for 16 h confirmed extensive transcriptional remodeling in S. aureus and revealed a conserved response across the three LAB treatments, including activation of stress, proteostasis, energy metabolism and arginine catabolism functions, together with repression of surface-associated, matrix-related, metal acquisition and virulence-associated pathways. In contrast, LAB transcriptomic responses were more moderate and strain-dependent, suggesting different metabolic, nutrient-acquisition and envelope-adaptation strategies during biofilm-associated interactions. Overall, these findings suggest that these LAB strains can displace mastitis-associated S. aureus from mature biofilms and promote a coordinated transcriptional shift toward stress adaptation and attenuation of virulence- and persistence-associated functions.
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BibTeX
@article{jurado2026transcriptomic,
title = {{Transcriptomic reprogramming and displacement of mastitis-associated Staphylococcus aureus biofilms by lactic acid bacteria}},
author = {Rubén Jurado and Rubén Jurado and Rubén Jurado and Angela França and Natalia Hernando and Natalia Hernando and Alberto Aragón and Alberto Aragón and Juan M. Rodríguez and Juan M. Rodríguez and Leonides Fernández and Leonides Fernández and Belén Orgaz and Belén Orgaz},
journal = {Frontiers in Cellular and Infection Microbiology},
year = {2026},
month = oct,
doi = {10.3389/fcimb.2026.1957508},
url = {https://doi.org/10.3389/fcimb.2026.1957508},
note = {CC BY},
}
RIS
TY - JOUR
TI - Transcriptomic reprogramming and displacement of mastitis-associated Staphylococcus aureus biofilms by lactic acid bacteria
AU - Rubén Jurado
AU - Rubén Jurado
AU - Rubén Jurado
AU - Angela França
AU - Natalia Hernando
AU - Natalia Hernando
AU - Alberto Aragón
AU - Alberto Aragón
AU - Juan M. Rodríguez
AU - Juan M. Rodríguez
AU - Leonides Fernández
AU - Leonides Fernández
AU - Belén Orgaz
AU - Belén Orgaz
PY - 2026
DA - 2026/10/26
JO - Frontiers in Cellular and Infection Microbiology
DO - 10.3389/fcimb.2026.1957508
UR - https://doi.org/10.3389/fcimb.2026.1957508
AB - Staphylococcus aureus is one of the main etiological agents of acute mastitis during lactation, and its ability to persist in biofilms can compromise conventional antimicrobial treatments. Lactic acid bacteria (LAB) have emerged as promising probiotic candidates for mastitis management, but the molecular mechanisms underlying their interaction with S. aureus remain poorly understood. This study aimed to evaluate the ability of three LAB strains (Limosilactobacillus fermentum I7, Limosilactobacillus reuteri 7SNG3–30 and Ligilactobacillus salivarius 22SNG3-30) to interfere with mature biofilms formed by two mastitis-associated S. aureus strains, SA4 and SA55, and to characterize the associated transcriptional responses. The LAB strains were able to colonize preformed 24-h S. aureus biofilms, eventually dominating the mixed-species communities and reducing the attached staphylococcal population. RT-qPCR showed limited transcriptional changes after 4 h of LAB exposure, followed by a broader 16-h response characterized by induction of the stress/adaptation marker uspA and repression of genes related to quorum sensing, virulence, biofilm matrix production and iron acquisition. RNA-seq analysis of SA4 biofilms exposed to LAB for 16 h confirmed extensive transcriptional remodeling in S. aureus and revealed a conserved response across the three LAB treatments, including activation of stress, proteostasis, energy metabolism and arginine catabolism functions, together with repression of surface-associated, matrix-related, metal acquisition and virulence-associated pathways. In contrast, LAB transcriptomic responses were more moderate and strain-dependent, suggesting different metabolic, nutrient-acquisition and envelope-adaptation strategies during biofilm-associated interactions. Overall, these findings suggest that these LAB strains can displace mastitis-associated S. aureus from mature biofilms and promote a coordinated transcriptional shift toward stress adaptation and attenuation of virulence- and persistence-associated functions.
SN - 2235-2988
ER -