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• W3208784503 abstract "Certaines bactéries Gram négatif sont tuées par l'action combinée de l'anticorps et du complément. L'antigène cible de l'anticorps serait un antigène « rugueux , commun aux souches lisses et rugueuses, mais qui serait masqué chez les souches lisses par le polysaccharide O, d'où la résistance relativement plus grande des souches lisses. La résistance dépend aussi de la distance séparant le substrat du complément du complexe antigène-anticorps. La nécessité de l'anticorps, bien établie dans le cas des souches lisses, a été discutée dans le cas des souches rugueuses ; l'interaction du LPS avec le complément ne requiert que des taux extrêmement faibles (et peut-être nuls) d'anticorps. L'anticorps bactéricide, naturel ou immun, prédomine dans les IgM. Son efficacité est augmentée par la présence d'une immunoconglutinine. Des « perforationsde 90–110 Å de diamètre, caractéristiques de l'action du complément, apparaissent sur le lipopolysaccharide qui constitue la membrane externe de la bactérie. Le lysozyme, non bactéricide par lui-même, favorise l'action bactéricide du complément. En l'absence du lysozyme, la mort cellulaire résulte d'une lésion primaire sur cette membrane externe causée par le complément et d'un dommage secondaire de la membrane plasmatique, probablement d'origine osmotique. Le lysozyme a un rôle fondamental dans la lyse : après l'action de la séquence totale du complément, le lysozyme agit sur la couche profonde mucopeptidique de la paroi bactérienne, et transforme les bactéries tuées en sphéroplastes ; ces derniers donnent des « ghosts , avec libération de β-D-galactosidase intra-cellulaire. L'activité bactéricide immune, dont la mesure est à la base de diverses épreuves de laboratoire, s'exerce aussi bien in vivo qu'in vitro, et présente des variations physiologiques. Dans les déficiences héréditaires en composant C2 chez l'homme, cette activité est peu altérée. A l'état pathologique, la susceptibilité augmentée aux infections est associée aux déficiences en anticorps, et exceptionellement à la déficience en complément. L'immunité naturelle envers les entérobactéries pathogènes paraît due à des types simplifés d'anticorps dirigés contre des antigènes « rugueuxcommuns à de nombreuses souches et espèces d'entérobactéries. L'immunoconglutinine a un rôle antiinfectieux. Le lysozyme scinde les liaisons β (1 → 4) à l'intérieur des peptidoglycanes des parois des bactéries aussi bien Gram négatif que Gram positif ; largement distribué dans l'organisme, il paraît constituer un mécanisme de la défense anti-bactérienne. L'activité bactéricide immune apparaît dès la vie intra-utérine chez les mammifères. Elle est observée chez la plupart des Vertébrés. Serum kills many gram-negative organisms by a reaction requiring complement and antibody against a cell envelope antigen. Smooth bacteria are significantly more resistant than rough organisms to the lethal action of the antibody-complement system. Smooth organisms differ from the rough ones in that they contain increased amounts of O-antigen in the lipopolysaccharide (LPS) of the cell wall. Several workers have suggested that a rough antigen is the target antigen of the bactericidal antibody but it is internal to the O-polysaccharide and thus protected by it in smooth organisms. Another explanation for the serum resistance is that the action of complement may occur too far from the lipid-containing substrate to cause wall damage. The requirement of antibody for killing smooth gram-negative bacteria has been demonstrated repeatedly. Several workers, however, have questioned the antibody requirement for killing rough bacteria. Furthermore some investigators have, as yet, been unable to show with certainty a requirement for antibody for the serum-mediated damage to isolated lipopolysaccharide. Natural and immune bactericidal antibodies are almost entirely found in the IgM fraction. The immunoconglutinin sera had significantly more bactericidal activity than normal sera. The complement components are activated by the formation of the antigen-antibody complex on the bacterial cell surface. The whole complement sequence of the presently recognized nine components is required for bacterial killing. Characteristic ultrastructural lesions or holes, which have approximately 90–110 Å diameter, are produced by complement on the outer lipopolysaccharide-containing membrane of the bacterial cell wall. This damage is not by itself bactericidal in the absence of lysozyme unless secondary damage of the inner, cytoplasmic membrane occurs as a consequence of the usually existing osmotic forces which become lethal in the presence of a defective cell wall. Gram-negative bacteria cannot be attacked by lysozyme alone. Lysozyme is not essential for the killing of gram-negative organisms by antibody and complement, but it can markedly potentiate the effect. In the absence of lysozyme, killed, rod-shaped organisms result ; with lysozyme present, the rigid peptidoglycan layer is degrated, yielding spheroplasts. Immune bacteriolysis requires all nine components of complement before lysozyme attacking of the rigid structure of the bacterial cell wall ; this leads to the formation of spheroplasts with the liberation of β-D-galactosidase. The subsequent conversion of spheroplasts to ghosts may be the result of instability of the exposed cell surface and not a direct effect of serum action. The assay of the immune bactericidal activity is frequently used in various laboratory tests. Immune bactericidal activity is observed in vivo as well as in vitro, and shows physiological variations. The individuals with inherited C2-deficiency have nevertheless sufficient C2 to support bactericidal function. Increased susceptibility to infection is associated with antibody deficiency, and exceptionally with deficiency in complement. The host could be able to modified enzymatically smooth virulent strains of Enterobacteriaceae in such a manner that they are rendered sensitive to serum factors that can react with rough antigens. Immunoconglutinin is believed to enhance the in vivo activity of antibody and complement in bactericidal activity. Lysozyme splits the β (1–4) linkages within the peptidoglycans from bacterial cell walls of gram-positive and gram-negative bacteria. The lysozyme is widely distributed in the organism ; it seems to contribute to the antibacterial defense. The immune bactericidal activity appears already during the intrauterine life in mammalia and is observed in most of the vertebrates. Bactericidal activity, as well as biological activities generated during the activation of complement, are parts of the humoral factors of the defense mechanism to infective aggression. An antigenic community between host and bacteria may initiate the apparition of autoantibodies. On the other hand, this antigenic parenty may act upon the host's resistance to infection." @default.
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• W3208784503 date "1972-01-01" @default.
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• W3208784503 title "Réactions bactéricide et bactériolytique immunes" @default.
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