Phospholipase C from Clostridium Perfringens Induces Human Platelet Aggregation in Plasma

Chiba

FEMS Microbiology Letters

1989

Ten distinct monoclonal antibodies (MAbs) against alpha toxin of Clostridium perfringens were produced by the fusion of SP2/O with spleen cells of micr immunized with alpha toxoid, and alpha toxin mixed with or without ethylenediamine‐tetraacetate (EDTA). The antibody activity was evaluated by antigen‐binding activity in an enzyme linked immunosorbent assay (ELISA), by phospholipase C (PLC)‐neutralizing activity using both egg yolk lecithin and p‐nitrophenylphosphoryl‐choline (PNPPC) hydrolysis reactions and by anti‐lethal activity in mice. Since the toxin‐neutralizing activities of each MAb were not parallel, it has been suggested that the three biological activities may not be located in the same site in the toxin molecule. This report also describes the development of a simple purification of the toxin by affinity chromatography and a sensitive immunoassay for quantitation of the toxin using the monoclonal antibody.

Section: Introductionmentioning

confidence: 99%

Monoclonal antibodies against alpha toxin of Clostridium perfringens

Chiba

FEMS Microbiology Letters

1989

Monoclonal antibodies against alpha toxin of Clostridium perfringens

Chiba

FEMS Microbiology Letters

1989

Ten distinct monoclonal antibodies (MAbs) against alpha toxin of Clostridium perfringens were produced by the fusion of SP2/O with spleen cells of mice immunized with alpha toxoid, and alpha toxin mixed with or without ethylenediamine-tetraacetate (EDTA). The antibody activity was evaluated by antigen-binding activity in an enzyme linked immunosorbent assay (ELISA), by phospholipase C (PLC)-neutralizing activity using both egg yolk lecithin and p-nitrophenylphosphoryl-choline (PNPPC) hydrolysis reactions and by anti-lethal activity in mice. Since the toxin-neutralizing activities of each MAb were not parallel, it has been suggested that the three biological activities may not be located in the same site in the toxin molecule. This report also describes the development of a simple purification of the toxin by affinity chromatography and a sensitive immunoassay for quantitation of the toxin using the monoclonal antibody.

The role of platelets in infective endocarditis

Ford

Douglas²

1997

Platelets

There is growing evidence that platelets play an important role in the development of infective endocarditis (IE). This review focuses on interactions between bacteria and platelets. Many types of microorganism are capable of causing endocarditis. The oral streptococci, particularly Streptococcus sanguis and S. oralis, remain the most common causative bacteria in IE but Staphylococcus aureus is becoming an increasingly important agent. Several species of bacteria and fungi are able to cause platelet aggregation in vitro, and there are indications that this ability is associated with the production of severe disease. Different bacteria appear to utilise different mechanisms of aggregation, and mechanisms for adhesion may be distinct from those responsible for aggregation. At least one commonly studied strain of S. sanguis apparently utilises the host's IgG and complement responses to induce platelet activation. IE may therefore be among the number of diseases in which immunological activation of platelets is thought to be of importance. Other bacterial strains have their own adhesins and agonists. The more virulent bacteria, notably the staphylococci, also possess proteolytic enzymes and may directly activate coagulation pathways, whereas less virulent, opportunistic pathogens, such as some streptococci and Candida albicans, may rely on interactions with host factors for colonisation and proliferation. It is proposed that platelets are involved in formation of the non-bacterial thrombotic vegetation (NBTV) and are necessary for the effective adhesion of bacteria to the NBTV, and that platelets also influence the persistence and clinical outcome of the disease through proliferation of the thrombotic vegetation. It is hypothesised that successful colonisation of the heart valves by a micro-organism depends on effective adhesion of the bacteria or fungi to platelets, in combination with the ability to induce platelet activation and aggregation.