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Dengue virus infection of human endothelial cells leads to chemokine production, complement activation, and apoptosis.
TLDR
It is shown that infection of human endothelial cells with DV induces the transcriptional up-regulation and secretion of RANTES and IL-8 and, in the presence of anti-dengue Abs, the formation of nonlytic complement complexes.
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Vascular leakage in severe dengue virus infections: a potential role for the nonstructural viral protein NS1 and complement.
TLDR
Complement activation mediated by NS1 leads to local and systemic generation of anaphylatoxins and SC5b-9, which may contribute to the pathogenesis of the vascular leakage that occurs in patients with DHF/DSS.
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Alpha-toxin of Staphylococcus aureus.
TLDR
Alpha-toxin, the major cytotoxic agent elaborated by Staphylococcus aureus, was the first bacterial exotoxin to be identified as a pore former and well-studied phenomena include the stimulation of arachidonic acid metabolism, triggering of granule exocytosis, and contractile dysfunction.
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Escherichia coli hemolysin may damage target cell membranes by generating transmembrane pores
TLDR
It is suggested that E. coli hemolysin may damage cell membranes by partial insertion into the lipid bilayer and generation of a discrete, hydrophilic transmembrane pore with an effective diameter of approximately 3 nm, caused by the insertion of toxin monomers into the target lipid bilayers.
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Delivery of proteins into living cells by reversible membrane permeabilization with streptolysin-O
TLDR
The presented method for introducing proteins into living cells should find multifaceted application in cell biology.
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Stimulation of monokine production by lipoteichoic acids
TLDR
Some species of LTAs are identified as inducers of monokine production in human monocytes, and kinetics of IL-1 beta and tumor necrosis factor alpha release elicited by LTAs closely resembled those observed following lipopolysaccharide application.
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Protein sorting in Plasmodium falciparum-infected red blood cells permeabilized with the pore-forming protein streptolysin O.
TLDR
In search of an experimental system that would allow dissection of the individual steps involved in transport from the parasite surface into the RBC cytosol, and an assessment of the molecular requirements for the process at the erythrocytic side of the vacuolar membrane, permeabilized infected RBCs with the pore-forming protein streptolysin O.
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Staphylococcal α Toxin
TLDR
Antibodies against α toxin become detectable in sera of all young adults, indicating that toxin production occurs in humans even in the absence of clinical disease, and constitutes the best-studied example of how a pore-forming toxin can contribute to microbial virulence.
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Mechanism of membrane damage by streptolysin-O
TLDR
Although cholesterol plays a key role in the initial binding of SLO to the membrane, it does not directly participate in the formation of the membrane-penetrating toxin channels, which is basically analogous to that mediated by previously studied channel formers.
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Staphylococcal alpha-toxin, streptolysin-O, and Escherichia coli hemolysin: prototypes of pore-forming bacterial cytolysins
TLDR
This review will compare properties of the three toxin prototypes, highlighting the similarities and also the differences in their structure, mode of binding, mechanism of pore formation, and the responses they elicit in target cells.
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