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At least 181 records · Page 10Linked to original sources
PubMed1982

Effects of diphtheria toxin and other exotoxins on oxidant generation by human and murine phagocytes.

Bacterial exotoxins such as diphtheria toxin (D.T.), staphylococcal alpha toxin and Leucocidin can powerfully activate granulocytes and macrophages as detected by production of chemiluminescence in presence of Luminol. Production of superoxide by granulocytes and of prostaglandin E2 in macrophages is also stimulated by D.T. In contrast with the known resistance of rodent parenchymal cells to the diphtheria toxin, human and rodent leucocytes have similar sensitivities to D.T.

Animals↗
PubMed2000

Immunotherapy against antibiotic-resistant bacteria: the Russian experience with an antistaphylococcal hyperimmune plasmaand immunoglobulin.

The Russian experience with the preparation and clinical application of an antitoxic antistaphylococcal hyperimmune plasma and immunoglobulin is described. The immunotherapies were developed in the late 1960s and put into widespread use in the Soviet Union for the prophylaxis and treatment of sepsis, pneumonia, and other conditions caused by an epidemic of antibiotic-resistant Staphylococcus aureus.

Animals↗
PubMed1999

Staphylococcal scalded skin syndrome in an adult associated with methicillin-resistant Staphylococcus aureus.

We report the first adult case of staphylococcal scalded skin syndrome (SSSS) due to methicillin-resistant Staphylococcus aureus (MRSA). This case is particularly unusual as the MRSA produced toxic shock syndrome toxin 1 and enterotoxin, but not exfoliatoxin. SSSS was originally described in neonates and is thought to result from exfoliatins which produce subcorneal splitting of the epidermis and are only produced by certain strains of S. aureus. This case reflects the range of toxins that can be associated with SSSS and the clinical manifestations of MRSA infection in adult patients.

Aged↗
PubMed2003

Death by a B cell superantigen: In vivo VH-targeted apoptotic supraclonal B cell deletion by a Staphylococcal Toxin.

Amongst the many ploys used by microbial pathogens to interfere with host immune responses is the production of proteins with the properties of superantigens. These properties enable superantigens to interact with conserved variable region framework subdomains of the antigen receptors of lymphocytes rather than the complementarity determining region involved in the binding of conventional antigens. To understand how a B cell superantigen affects the host immune system, we infused protein A of Staphylococcus aureus (SpA) and followed the fate of peripheral B cells expressing B cell receptors (BCRs) with VH regions capable of binding SpA. Within hours, a sequence of events was initiated in SpA-binding splenic B cells, with rapid down-regulation of BCRs and coreceptors, CD19 and CD21, the induction of an activation phenotype, and limited rounds of proliferation. Apoptosis followed through a process heralded by the dissipation of mitochondrial membrane potential, the induction of the caspase pathway, and DNA fragmentation. After exposure, B cell apoptotic bodies were deposited in the spleen, lymph nodes, and Peyer's patches. Although in vivo apoptosis did not require the Fas death receptor, B cells were protected by interleukin (IL)-4 or CD40L, or overexpression of Bcl-2. These studies define a pathway for BCR-mediated programmed cell death that is VH region targeted by a superantigen.

Animals↗
PubMed1975

Studies of the mechanism of epidermal injury by a Staphylococcal epidermolytic toxin.

Experimental animal models of the two forms of toxic epidermal necrolysis have been reviewed: a murine model of staphylococcal-induced epidermolysis and a hamster model of graft-versus-host disease. In the former, a protein exotoxin, epidermolysin, has been purified and characterized. The exotoxin has a molecular weight of approximately 30,000 and causes a split beneath the granular layer. It is effective at 3 times 10(-12) moles. Epidermolysin does not require an intact complement system for its action since B10D2 mice deficient in C5 or mice injected with the decomplementing agent in cobra venom factor were susceptible to its epidermolytic effects. Neither are immunocompetent thymocytes required for the action of the toxin since hairless, athymic adult (nu/nu) mice are susceptible. A few reports of epidermolysis due to an exotoxin of group I Staphylococcus aureus have appeared. This toxin is antigenically different from the exotoxin of group II organisms. A model of drug-induced toxic epidermal necrolysis has been described in hamsters, but the toxic principle released from sensitized lymphoid cells has not yet been characterized.

Animals↗
PubMed1969

Effect of formaldehyde on the immunochemical and biological activity of staphylococcal enterotoxin B.

Staphylococcal enterotoxin B was treated with 0.15 or 0.3% formaldehyde at 37 C and pH 7.3. As early as 8 hr after addition of HCHO, the toxin was unable to precipitate as much antibody from antiserum as untreated toxin; greater amounts of treated toxin were required to reach equivalence and to inhibit precipitation. With increasing time, its reactivity decreased so that at 32 weeks it could precipitate only 20% as much antibody as untreated toxin. When other factors were kept constant, the degree of inactivation increased as the HCHO concentration increased from 0.6 to 1.4%. Treated toxin gave a "reaction of partial identity" by the Ouchterlony double-immunodiffusion technique. The emetic effect of the toxin for the monkey remained essentially unchanged for about 48 hr of treatment, but the amount required to cause death by the intravenous route increased from 25 to over 1,000 mug/kg of body weight. HCHO destroyed the pyrogenic effect for rabbits. The treated toxin remained immunogenic for rabbits even after 4 to 5 weeks of exposure to 0.3% HCHO at 37 C.

Animals↗
PubMed1979

Immunologic evidence that staphylococcal alpha toxin is oriented on membranes.

Antibodies to staphylococcal alpha toxin were separated into two distinct populations. One population prevented binding of alpha toxin onto erythrocyte membranes. The other population neutralized after the toxin was bound onto erythrocytes and thereby brought about an indirect hemagglutination reaction. The data suggest that alpha toxin has a membrane-binding region.

Animals↗