Comparative transcriptional analysis of homologous pathogenic and non-pathogenic Lawsonia intracellularis isolates in infected porcine cells.
Authors: Vannucci Fabio A, Foster Douglas N, Gebhart Connie J
Journal: PloS one
Summary
# Editorial Summary: Lawsonia intracellularis Virulence Factors in Proliferative Enteropathy Proliferative enteropathy, caused by *Lawsonia intracellularis*, remains endemic in pigs and represents an emerging disease threat in horses, yet the bacterial mechanisms driving pathogenesis remain poorly characterised. Vannucci and colleagues employed high-throughput RNA sequencing to compare gene expression profiles between a virulent low-passage isolate (passage 10) and an attenuated laboratory variant (passage 60) during cellular infection, identifying which bacterial genes might encode critical virulence determinants. The pathogenic isolate uniquely expressed 401 genes absent in the non-pathogenic variant, predominantly encompassing plasmid-encoded sequences and genes controlling membrane transport, stress responses and transcriptional regulation; notably, the entire plasmid A repertoire was silenced in the attenuated strain, suggesting its central role in virulence. Amongst the 319 genes expressed by both variants, transcription levels showed no significant difference but demonstrated strong positive correlation (r² = 0.81), indicating that virulence attenuation occurs through selective gene silencing rather than genetic loss. These findings provide the first comprehensive transcriptional map of *L. intracellularis* pathogenesis, identifying specific genetic targets—particularly plasmid A genes and stress-response regulators—that warrant mechanistic investigation for developing diagnostic markers and improved control strategies in affected equine and porcine populations.
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Practical Takeaways
- •Proliferative enteropathy in horses involves complex virulence mechanisms centered on plasmid-encoded genes and membrane transport systems — understanding these may improve diagnostic and control strategies
- •The finding that pathogens lose virulence through gene silencing (not genetic loss) suggests potential therapeutic targets and explains why some field isolates behave differently than laboratory strains
- •This foundational research on L. intracellularis virulence mechanisms should inform development of more effective vaccines and treatment protocols for equine proliferative enteropathy
Key Findings
- •401 genes were exclusively expressed in pathogenic (passage 10) L. intracellularis variant compared to non-pathogenic (passage 60) variant
- •Plasmid A genes and membrane transporter/stress response genes were predominantly responsible for differential pathogenic expression
- •Gene silencing mechanisms appear to attenuate virulence during multiple cell passages in vitro
- •319 commonly expressed genes showed strong positive correlation (r²=0.81) between pathogenic and non-pathogenic variants, suggesting phenotype differences are due to gene expression switching rather than gene loss