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Forschungsdatenbank PMU-SQQUID

Microvesicle shedding and lysosomal repair fulfill divergent cellular needs during the repair of streptolysin O-induced plasmalemmal damage.
Atanassoff, AP; Wolfmeier, H; Schoenauer, R; Hostettler, A; Ring, A; Draeger, A; Babiychuk, EB;
PLoS One. 2014; 9(2): e89743
Originalarbeiten (Zeitschrift)

PMU-Autor/inn/en

Wolfmeier Heidi

Abstract

Pathogenic bacteria secrete pore-forming toxins that permeabilize the plasma membrane of host cells. Nucleated cells possess protective mechanisms that repair toxin-damaged plasmalemma. Currently two putative repair scenarios are debated: either the isolation of the damaged membrane regions and their subsequent expulsion as microvesicles (shedding) or lysosome-dependent repair might allow the cell to rid itself of its toxic cargo and prevent lysis. Here we provide evidence that both mechanisms operate in tandem but fulfill diverse cellular needs. The prevalence of the repair strategy varies between cell types and is guided by the severity and the localization of the initial toxin-induced damage, by the morphology of a cell and, most important, by the incidence of the secondary mechanical damage. The surgically precise action of microvesicle shedding is best suited for the instant elimination of individual toxin pores, whereas lysosomal repair is indispensable for mending of self-inflicted mechanical injuries following initial plasmalemmal permeabilization by bacterial toxins. Our study provides new insights into the functioning of non-immune cellular defenses against bacterial pathogens.


Useful keywords (using NLM MeSH Indexing)

Actin Cytoskeleton/metabolism

Bacterial Proteins/pharmacology

Cell Line, Tumor

Cell Membrane/drug effects

Cell Membrane/physiology*

Cell Survival

Cell-Derived Microparticles/physiology*

HEK293 Cells

Humans

Immunity, Innate

Lysosomes/physiology*

Membrane Fusion

Myosins/metabolism

Streptolysins/pharmacology*