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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:Leptospirosis, an emerging zoonotic disease with worldwide distribution, is caused by spirochetes belonging to the genus Leptospira. More than 500,000 cases of severe leptospirosis are reported annually, with .10% of these being fatal. Leptospires can survive for weeks in suitably moist conditions before encountering a new host. Reservoir hosts, typically rodents, exhibit little to no signs of disease but shed large numbers of organisms in their urine. Transmission occurs when mucosal surfaces or abraded skin come into contact with infected urine or urine-contaminated water or soil. In humans, leptospires can cause a variety of clinical manifestations, ranging from asymptomatic or mild fever to severe icteric (Weil’s) disease and pulmonary haemorrhage. Currently, little is known about how Leptospira persist within a reservoir host. Prior in vitro studies have suggested that leptospires alter their transcriptomic and proteomic profiles in response to environmental signals encountered during mammalian infection. However, no study has examined gene expression by leptospires within a mammalian host-adapted state. To obtain a more faithful representation of how leptospires respond to host-derived signals, we used RNA-Seq to compare the transcriptome of L. interrogans cultivated within dialysis membrane chambers (DMCs) implanted into the peritoneal cavities of rats with that of organisms grown in vitro. In addition to determining the relative expression levels of ‘‘core’’ housekeeping genes under both growth conditions, we identified 166 genes that are differentially-expressed by L. interrogans in vivo. Our analyses highlight physiological aspects of host adaptation by leptospires relating to heme uptake and utilization. We also identified 11 novel non-coding transcripts that are candidate small regulatory RNAs. The DMC model provides a facile system for studying the transcriptional and antigenic changes associated with mammalian host-adaption, selection of targets for mutagenesis, and the identification of previously unrecognized virulence determinants. Transcriptome analysis of L. interrogans Copenhageni FIOCRUZ L1-130 using RNA from 2 different conditions using RNA-seq. Also, the reproducibility and robustness of data is ensured by three biological replicates from each condition.

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

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