首页> 外文期刊>Medycyna Weterynaryjna >Virulence factors of Actinobacillus pleuropneumoniaeOriginal Title (non-English) Czynniki zjadliwosci Actinobacillus pleuropneumoniae [Polish]
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Virulence factors of Actinobacillus pleuropneumoniaeOriginal Title (non-English) Czynniki zjadliwosci Actinobacillus pleuropneumoniae [Polish]

机译:胸膜肺炎放线杆菌的毒性因子原始名称(非英语)Czynniki zjadliwosci胸膜肺炎放线杆菌[波兰语]

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The virulence factors of Actinobacillus pleuropneumoniae (App) have been described. The most important among them are: Apx toxins, proteases, lipopolysaccharides (LPS), capsule polysaccharides (CPS), outer membrane proteins and adhesins. All App strains possess CPS, which facilitates their invasion by protecting bacteria from the defense of the host immune system (phagocytosis and lysis). It also prevents the opsonization and removing of bacteria from the respiratory tract. Being a component of the external membrane, LPS induces production of the tumor necrosis factor, interleukins, interferons, activated oxygen compounds, prostaglandins, platelet activating factor and leukotrienes. Proteases released by App have the capacity of IgA cleavage and degradation of hemoglobin. These facilitate mucosal colonization and acquisition of iron ions necessary for the survival of bacteria. Actinobacillus pleuropneumoniae synthesizes four toxins: Apx I, ApxI I, ApxIII and ApxIV. They have the ability to form pores in biological membranes and stimulate secretion of proinflammatory mediators. They possess hemolytic and cytotoxic capacities. Apx toxins damage endothelial cells and activate the thrombocytes which result in microclot formation leading to necrosis. Apx toxins are also highly immunogenic. They play a dominant role in the pathogenesis of swine pleuropneumonia. The lack of Apx genes definitely causes a loss of bacterial virulence. Nevertheless, other App structures may also significantly affect the course of App infection.
机译:已经描述了胸膜肺炎放线杆菌(Appino)的毒力因子。其中最重要的是:Apx毒素,蛋白酶,脂多糖(LPS),荚膜多糖(CPS),外膜蛋白和粘附素。所有App菌株均具有CPS,可通过保护细菌免受宿主免疫系统的防御(吞噬作用和裂解作用)来促进其入侵。它还可以防止调理作用和从呼吸道清除细菌。作为外膜的一部分,LPS诱导肿瘤坏死因子,白介素,干扰素,活性氧化合物,前列腺素,血小板活化因子和白三烯的产生。 App释放的蛋白酶具有IgA裂解和血红蛋白降解的能力。这些促进了粘膜定居和细菌生存所必需的铁离子的获取。胸膜肺炎放线杆菌合成四种毒素:Apx I,ApxI I,ApxIII和ApxIV。它们具有在生物膜中形成孔并刺激促炎性介质分泌的能力。它们具有溶血和细胞毒性的能力。 Apx毒素会破坏内皮细胞并激活血小板,从而导致微凝块形成,从而导致坏死。 Apx毒素也是高度免疫原性的。它们在猪胸膜肺炎的发病机理中起主要作用。 Apx基因的缺乏肯定会导致细菌毒力的丧失。但是,其他App结构也可能会严重影响App感染的过程。

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