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Interplay between two peroxide stress regulators in the oxidative stress response and virulence of pathogenic Leptospira

ABSTRACT: Pathogenic Leptospira spp. are the causative agents of the zoonotic disease leptospirosis. During infection, Leptospira are confronted with deadly reactive oxygen species (ROS). Withstanding ROS produced by the host innate immunity is an important strategy evolved by pathogenic Leptospira for persisting in and colonizing hosts. The peroxide stress regulator, PerRA, represses genes involved in ROS defenses in L. interrogans. We have identified an ORF encoding a putative second PerR in pathogenic Leptospira that we named PerRB. We have determined the transcriptomic profil of a single perRB and a double perRAperRB mutants. The concomitant inactivation of perRA and perRB has a pleiotropic effect on the transcriptomic profil of L. interrogans. The lack of both PerRA and PerRB regulators led to the differential expression of several virulence-associated genes and a loss of virulence. Our findings provide new insights into a new regulatory network that controls virulence and host colonization.

ORGANISM(S): Leptospira interrogans serovar Manilae

PROVIDER: GSE158051 | GEO | 2021/10/07

REPOSITORIES: GEO

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Project description:The life-threatening pathogen Leptospira interrogans navigates a dual existence: surviving in environmental reservoirs and infecting mammalian hosts. Leptospira biofilm formation is thought to be an important survival strategy in environmental contexts and may also contribute to the persistence of leptospirosis in maintenance hosts. Examining the correlation between biofilm formation and the virulence of pathogenic strains might improve our comprehension of the epidemiology of leptospirosis. To further explore Leptospira’s survival strategy, our study focused on elucidating the biological state of pathogenic Leptospira within biofilms, particularly aiming to uncover the adaptations and regulatory mechanisms that are involved in such complex microenvironments. To determine the transcriptional profile of pathogenic Leptospira in biofilm, we compared the genome-wide transcriptomic profiles in late biofilms (21 days old) with those in exponential planktonic cultures (5 days old), revealing a pronounced transcriptomic shift. While genes linked to motility, energy production, and metabolism were downregulated, those governing the general stress response, defense against metal stress, and redox homeostasis showed a significant upsurge, hinting at a tailored defensive strategy against stress in late biofilms. A standout finding was the increased expression of the csoR, copZ, and copA locus, integral to copper ion stress response in other bacterial genera, suggesting a unique adaptation to metal-induced stress. Further, despite a reduced metabolic state in biofilms, their disruption swiftly restored metabolic activity. Crucially, bacteria either in late biofilms or resulting from biofilm disruption retained virulence in a hamster infection model, defying the notion that biofilm maturation abolishes pathogenicity. In summary, our study highlights Leptospira's adaptive equilibrium in biofilms: minimizing cellular energy expenditure to conserve resources, potentially aiding in withstanding stresses while maintaining its pathogenicity. These insights are important for explaining the survival strategies of Leptospira, revealing that a biofilm lifestyle may confer an advantage in maintaining virulence. This understanding is essential for managing leptospirosis across both environmental reservoirs and mammalian hosts.

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Interplay between two peroxide stress regulators in the oxidative stress response and virulence of pathogenic Leptospira

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