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      Differential gene expression profile of Shigella dysenteriae causing bacteremia in an immunocompromised individual


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          Shigella species has varying levels of virulence gene expression with respect to different sites of infection. In this study, the differential gene expression of S. dysenteriae in response to its site of infection was analyzed by transcriptomics.


          This study includes four clinical Shigella isolates. Transcriptomics was done for the stool and blood samples of a single patient. Isolates were screened for the presence of antimicrobial resistance genes.


          The majority of genes involved in invasion were highly expressed in the strain isolated from the primary site of infection. Additionally, antimicrobial resistance ( dhfr1A, sulII, bla OXA. bla CTX-M-1 and qnrS) genes were identified.


          This study provides a concise view of the transcriptional expression of clinical strains and provides a basis for future functional studies on Shigella spp.

          Lay abstract

          Shigella infection is restricted to the gastrointestinal tract and rarely causes fatal extra-intestinal complications like bacteremia. There are limited studies available from India on molecular characterization of Shigella spp. In this study, we characterized four Shigella isolates obtained from bloodstream infections. Shigella spp. isolated from the stool and blood of one representative patient was further sequenced to study the differential gene expression profile. The differential protein expression by S. dysenteriae observed in this study demonstrates that it has a specific response to particular intracellular environments. Further, the in vivo mechanism of Shigellae invasion are difficult to fully study until the intracellular environment is mimicked in vitro. To the best of our knowledge, this is the first Indian study that compared the gene expression profile of clinical Shigella strains.

          Most cited references29

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          How bacterial pathogens colonize their hosts and invade deeper tissues.

          Bacterial pathogens have evolved a wide range of strategies to colonize and invade human organs, despite the presence of multiple host defense mechanisms. In this review, we will describe how pathogenic bacteria can adhere and multiply at the surface of host cells, how some bacteria can enter and proliferate inside these cells, and finally how pathogens may cross epithelial or endothelial host barriers and get access to internal tissues, leading to severe diseases in humans.
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            Genome dynamics and diversity of Shigella species, the etiologic agents of bacillary dysentery

            The Shigella bacteria cause bacillary dysentery, which remains a significant threat to public health. The genus status and species classification appear no longer valid, as compelling evidence indicates that Shigella, as well as enteroinvasive Escherichia coli, are derived from multiple origins of E.coli and form a single pathovar. Nevertheless, Shigella dysenteriae serotype 1 causes deadly epidemics but Shigella boydii is restricted to the Indian subcontinent, while Shigella flexneri and Shigella sonnei are prevalent in developing and developed countries respectively. To begin to explain these distinctive epidemiological and pathological features at the genome level, we have carried out comparative genomics on four representative strains. Each of the Shigella genomes includes a virulence plasmid that encodes conserved primary virulence determinants. The Shigella chromosomes share most of their genes with that of E.coli K12 strain MG1655, but each has over 200 pseudogenes, 300∼700 copies of insertion sequence (IS) elements, and numerous deletions, insertions, translocations and inversions. There is extensive diversity of putative virulence genes, mostly acquired via bacteriophage-mediated lateral gene transfer. Hence, via convergent evolution involving gain and loss of functions, through bacteriophage-mediated gene acquisition, IS-mediated DNA rearrangements and formation of pseudogenes, the Shigella spp. became highly specific human pathogens with variable epidemiological and pathological features.
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              Cold Shock Proteins: A Minireview with Special Emphasis on Csp-family of Enteropathogenic Yersinia

              Bacteria have evolved a number of mechanisms for coping with stress and adapting to changing environmental conditions. Many bacteria produce small cold shock proteins (Csp) as a response to rapid temperature downshift (cold shock). During cold shock, the cell membrane fluidity and enzyme activity decrease, and the efficiency of transcription and translation is reduced due to stabilization of nucleic acid secondary structures. Moreover, protein folding is inefficient and ribosome function is hampered. Csps are thought to counteract these harmful effects by serving as nucleic acid chaperons that may prevent the formation of secondary structures in mRNA at low temperature and thus facilitate the initiation of translation. However, some Csps are non-cold inducible and they are reported to be involved in various cellular processes to promote normal growth and stress adaptation responses. Csps have been shown to contribute to osmotic, oxidative, starvation, pH and ethanol stress tolerance as well as to host cell invasion. Therefore, Csps seem to have a wider role in stress tolerance of bacteria than previously assumed. Yersinia enterocolitica and Yersinia pseudotuberculosis are enteropathogens that can spread through foodstuffs and cause an enteric infection called yersiniosis. Enteropathogenic Yersinia are psychrotrophs that are able to grow at temperatures close to 0°C and thus they set great challenges for the modern food industry. To be able to efficiently control psychrotrophic Yersinia during food production and storage, it is essential to understand the functions and roles of Csps in stress response of enteropathogenic Yersinia.

                Author and article information

                Future Sci OA
                Future Sci OA
                Future Science OA
                Future Science Ltd (London, UK )
                29 January 2020
                April 2020
                29 January 2020
                : 6
                : 4
                : FSO456
                [1 ]Department of Clinical Microbiology, Christian Medical College, Vellore 632004, India
                Author notes
                [* ]Author for correspondence: Tel.: +91 944 221 0555; vbalaji@ 123456cmcvellore.ac.in
                © 2020 Balaji Veeraraghavan

                This work is licensed under the Creative Commons Attribution 4.0 License

                : 23 October 2019
                : 06 January 2020
                : 29 January 2020
                Page count
                Pages: 9
                Short Communication

                gene expression,icsa,invasive,rna-seq analysis,shigella
                gene expression, icsa, invasive, rna-seq analysis, shigella


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