Staphylococcus aureus induces miR-21 expression to promote bacterial persistence during nasal colonisation
Year: 2025
Type: article
Abstract: Staphylococcus aureus nasal colonisation is commonplace among healthy individuals, yet the immune mechanisms enabling bacterial persistence remain unclear. S. aureus drives local immunosuppression during nasal colonisation to facilitate persistence. This study reveals that S. aureus subverts microRNA-21 activity to promote IL-10 production within nasal tissue, while simultaneously impeding local pro-inflammatory responses. MiR-21 activity helps establish a S. aureus -induced immunosuppressive microenvironment which supports S. aureus persistence. Macrophages, which are key IL-10 producers, rapidly upregulate miR-21 upon S. aureus exposure.MiR-21 expression also coincides with an increase in intracellular survival of S. aureus within macrophages. Furthermore, S. aureus represses macrophage glycolysis to promote intracellular survival, which is dependent upon miR-21. Upon S. aureus colonisation, miR-21 −/− mice demonstrate an overall improved bacterial clearance compared to their WT counterparts. These findings place the targeting of miR-21, which controls glycolytic activity in macrophages, as a potential avenue to reducing bacterial persistence during S. aureus colonisation.
Source: Clinical Immunology
Authors: Alanna M. Kelly, Emilio G. Vozza, Brenda Morris, Seán C. Cahill, Charlotte M. Leane, Sinéad C. Corr, Rachel M. McLoughlin
Institutions: Trinity College Dublin, University College Cork
Language: English
Subfield: Infectious Diseases
Field: Medicine
Domain: Health Sciences
Open Access status: hybrid
Estimated APC paid: $4,400
Awards: Profiling immune signatures predictive of outcome in Staphylococcus aureus infection: Advancing next generation vaccine design, G3649624167, Staphylococcus aureus induced immunosuppressive memory: consequences for bug and for host, Exploring miR-21 in the dialogue between the microbiome and immunity to decipher mechanisms of disease
OpenAlex ID: W4413825486
