The impact of DeoRF on Listeria monocytogenes stress tolerance and survival.

Abstract

Listeria monocytogenes, a significant foodborne pathogen, is known for its remarkable adaptability to diverse environments through a genomic regulatory network that coordinates metabolic activities and stress responses. However, many of these genomic elements remain poorly understood. This study investigates the role of deoRF, a previously understudied member of the DeoR-family, in oxidative tolerance, intracellular infection, and virulence. Interestingly, the F2365ΔdeoRF strain showed no significant growth defects in minimal media with glucose, fructose, or sucrose, suggesting that DeoRF does not play a critical role in the uptake or metabolism of these sugars. Results showed that DeoRF plays a significant role in the ability of L. monocytogenes to adapt to oxidative stress. Additionally, DeoRF contributed significantly to cell-to-cell spread in L2 fibroblast cells, intracellular replication in macrophage cells, and virulence in mice following both intravenous and oral infection models. Transcriptomic analysis further revealed that deletion of deoRF caused downregulation of propanediol utilization, transcription regulators, phosphotransferase systems (PTS), complex networks of transcriptional regulators, and proteases genes. Conversely, sigma B regulator genes were upregulated in the ΔdeoRF strain. This study demonstrates that L. monocytogenes DeoRF contributes to pathogenicity and stress adaptation, and it is an important contributor to the complex listerial regulatory network.