IndraLab

Statements


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"Collaboration of SLO with other toxins may be critical to induce PMN necrosis as similarly mechanism has been reported XREF_BIBR, although it remains to be examined whether there exist explore interaction associated molecules on both host and bacterial membrane is needed."

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"The present study also uncovers that increased activity of SLO from invasive GAS isolates induces rapid and extensive necrosis to human PMN."

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"To delineate the cellular process that is triggered by SLO and SLS delivery the involvement of autophagy, apoptosis, and necrosis that are affected by the hemolysin toxins and were shown to be linked to GAS pathogenesis was examined."

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"In a further approach, we confirmed the passive release of Dnase1 from necrotic hepatocytes by inducing acute hepatocellular necrosis by a single injection of 100 μl SLO dissolved in PBS (20 μg/ml) di[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"Mutations in the gene caused an increased expression of various virulence genes; the upregulation of streptolysin O (SLO) induced necrosis of neutrophils and prompted the escape of csrS mutated strains from being killed by neutrophils, resulting in increased virulence in lethality in the mouse model XREF_BIBR."

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"SLO not only induces the necrosis of neutrophils through pore formation but also translocates the effector protein Nga into the host cytosol in a pore formation independent manner, thereby promoting intracellular survival in macrophages and epithelial cells."

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"In our previous study, using the Transwell system, we showed that SLO, which causes necrosis in neutrophils, and an IL-8 protease of ScpC are important for bacterial resistance to killing by neutrophils XREF_BIBR."