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Leptospira rLRR20 stimulates gene expressions in HK2 cell

ABSTRACT: Leptospires are highly motile bacteria that migrate from the breached skin to blood circulation of in human, allowing for their rapid dissemination and subsequent colonization of the liver, lungs, and kidneys. Pathogenic Leptospira contained numerous leucine-rich repeat (LRR) genes compared to non-pathogenic species that acted as virulence factors. The functions of the LRR proteins are still unknown and the relative responses of the host cell provided clear evidence that the regulation of host cell during Leptospirosis. We used microarrays to observation the global gene expression of human kidney epithelial cell (HK2 cell) under the treatment of rLRR20 protein.

ORGANISM(S): Homo sapiens

PROVIDER: GSE155061 | GEO | 2021/03/24

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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Leptospira rLRR20 stimulates gene expressions in HK2 cell

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