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  • 1
    In: EMBO Journal, 02 July 2018, Vol.37(13), pp.n/a-n/a
    Description: Long non‐coding s (lncs) play important roles in many cellular pathways, but their contribution to the defense of eukaryotic cells against pathogens remains poorly understood. A new study from Imamura in reports that infection in human cells impacts nuclear decay, which in turn drives the accumulation of otherwise unstable nuclear lncs, some of which may have protective effects against this common bacterial pathogen. These unexpected findings demand more efforts to fully decrypt the molecular functions of lncs in innate and adaptive immunity. infection impairs the nuclear RNA decay machinery in human cells, increasing the abundance of long non‐coding RNAs with a role in innate immunity.
    Keywords: Pathogens ; Immunity ; Infections ; Pathogens ; Molecular Chains ; Salmonella ; Bacterial Infections ; Pathogens ; Ribonucleic Acid–RNA ; Ribonucleic Acid–RNA ; Adaptive Immunity;
    ISSN: 0261-4189
    E-ISSN: 1460-2075
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  • 2
    In: EMBO Journal, 03 December 2018, Vol.37(23), pp.n/a-n/a
    Description: While mucosal inflammation is a major source of stress during enteropathogen infection, it remains to be fully elucidated how the host benefits from this environment to clear the pathogen. Here, we show that host stress induced by different stimuli mimicking inflammatory conditions strongly reduces the binding of to epithelial cells. Mechanistically, stress activates acid sphingomyelinase leading to host membrane remodeling. Consequently, knockdown or pharmacological inhibition of the acid sphingomyelinase blunts the stress‐dependent inhibition of binding to host cells. Interestingly, stress caused by intracellular replication also results in remodeling of the host cell membrane, and , which precludes re‐infection by this and other non‐motile pathogens. In contrast, Typhimurium overcomes the shortage of permissive entry sites by gathering effectively at the remaining platforms through its flagellar motility. Overall, our findings reveal host membrane remodeling as a novel stress‐responsive cell‐autonomous defense mechanism that protects epithelial cells from infection by non‐motile bacterial pathogens. Stress‐induced host membrane remodeling constitutes a novel cell‐autonomous defensive mechanism that protects epithelial cells from infection by and other non‐motile bacterial pathogens. Host oxidative stress strongly reduces S. flexneri binding to epithelial cells. Stress leads to host membrane remodeling, via activation of the acid sphingomyelinase by the MAPK p38 pathway, resulting in the formation of ceramide domains. Intracellular Shigella replication induces remodeling of the host cell membrane, in vitro and in vivo. Stress‐induced host membrane remodeling precludes re‐infection by non‐motile pathogens; motile pathogens are able to overcome this barrier through flagellar motility. Host membrane remodeling is a cell‐autonomous defense mechanism that protects epithelial cells from infection by .
    Keywords: Acid Sphingomyelinase ; Host Stress Response ; Membrane Remodeling ; Salmonella ; Shigella
    ISSN: 0261-4189
    E-ISSN: 1460-2075
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