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Life sciences · Journal article
Biofilm · August 26, 2026
Early or partial results. Treat as a signal, not a conclusion.
This mechanistic study demonstrates that a plasmid-encoded mrkABCDF gene cluster in Salmonella Thompson promotes biofilm formation, stress tolerance, and in vivo invasiveness through type 3 fimbriae. The work is grounded in a single clinical isolate with severe diabetic foot infection and uses systematic genetic perturbation to map the mrk cluster's contribution, but lacks multicenter validation, quantified effect sizes for clinical outcomes, or evidence from multiple strains.
Mechanistic study using CRISPR/Cas9 knockout, plasmid curing, targeted gene deletion, and genetic complementation in single clinical isolate with in vivo murine infection model. Clinical isolate from 58-year-old diabetic patient with severe refractory foot ulcer infection at tertiary hospital in China; laboratory-derived strains and murine hosts used for mechanistic studies.. Intervention: Presence of plasmid-encoded mrkABCDF gene cluster within Tn6011 transposon on IncX1-type plasmid; genetic knockouts and complementation of individual mrk genes.. Compared with: mrk-negative derivatives created via transposon deletion, plasmid curing, and targeted gene knockouts; complementation restored mrk function.. China (clinical isolate source); murine studies location not specified in excerpt..
Loss of mrk gene cluster resulted in profound reduction in biofilm biomass with concomitant increase in bacterial motility Type 3 fimbriae detected exclusively on surface of mrk-positive cells mrk expression enhanced bacterial tolerance to desiccation and oxidative stresses
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The identification of plasmid-encoded mrk as a virulence determinant in Salmonella Thompson may inform understanding of biofilm-associated infections and suggests carbapenems as a potential therapeutic strategy; however, clinical utility requires validation across multiple strains and patient cohorts.
Single clinical isolate with laboratory-based mechanistic studies using genetic manipulation; lacks clinical trial data, comparative clinical outcomes, or multi-strain validation to support clinical practice change.
As stated by the source record.
Quoted from the source exactly as published.
The identification of plasmid-encoded mrk as a virulence determinant in Salmonella Thompson may inform understanding of biofilm-associated infections and suggests carbapenems as a potential therapeutic strategy; however, clinical utility requires validation across multiple strains and patient cohorts.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
Biofilm formation is a fundamental survival strategy that enables bacterial persistence across diverse environments and hosts. While the mrk gene cluster encoding type 3 fimbriae is a well-established determinant of biofilm formation in Klebsiella pneumoniae, its presence and functional significance in Salmonella enterica remains poorly defined. In this study, we identified a plasmid-encoded mrkABCDF gene cluster carried on a highly conjugative IncX1 plasmid in a clinical Salmonella Thompson isolate. Using CRISPR/Cas9-mediated knockout of the mrk-containing Tn6011 transposon, plasmid curing, targeted gene deletion, and genetic complementation, we systematically dissected the contribution of mrkABCDF genes to biofilm development and associated phenotypes. Loss of the mrk gene cluster resulted in a profound reduction in biofilm biomass and a concomitant increase in bacterial motility. Type 3 fimbriae were detected exclusively on the surface of mrk-positive cells, confirming their structural role in surface attachment. The mrk operon was strongly expressed from an IS1-associated promoter, bypassing canonical MrkH-dependent regulation. Functionally, mrk expression enhanced bacterial tolerance to desiccation and oxidative stresses, and reduced susceptibility to macrophage phagocytosis. In vivo, mrk-positive strains exhibited enhanced gastrointestinal colonization and tissue invasion. Notably, carbapenems exhibited exceptional efficacy in inhibiting mrk-mediated biofilm formation, indicating their superior potential for treating biofilm-associated infections. Our findings demonstrate that plasmid-encoded mrkABCDF genes can act as key architectural and functional determinants of biofilm formation in Salmonella enterica. The horizontal dissemination of mrk-carrying IncX1 plasmids may promote the emergence of biofilm-adapted Salmonella lineages with enhanced environmental persistence and host colonization potential.
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