首页> 外文期刊>Infection and immunity >Elongated versions of Vlp surface lipoproteins protect Mycoplasma hyorhinis escape variants from growth-inhibiting host antibodies.
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Elongated versions of Vlp surface lipoproteins protect Mycoplasma hyorhinis escape variants from growth-inhibiting host antibodies.

机译:Vlp表面脂蛋白的延长形式可以保护猪支原体逃逸变体免受生长抑制宿主抗体的侵害。

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Variation in Vlp surface proteins of Mycoplasma hyorhinis was evaluated in terms of its role in determining susceptibility of organisms to growth inhibition by host antibodies (Abs). High-frequency switching of Vlp surface lipoproteins has been studied in isogenic lineages of M. hyorhinis SK76. In these lineages, the products of three genes, vlpA, vlpB, and vlpC, are subject to phase and size variation in vitro, which occur through distinct mutator elements that independently govern the expression of each vlp gene (promoter mutations) or the size of the vlp gene product (by intragenic expansion or contraction of a 3' region containing tandem repeats). Isogenic clonal variants of M. hyorhinis SK76 expressing distinct profiles of Vlp products were assessed for their susceptibility to complement-independent growth inhibition by serum Abs of swine experimentally infected with the arthritigenic SK76 strain. Invariably, variants expressing longer versions of VlpA, VlpB, or VlpC (each expressed individually) were completely resistant to host immune serum Abs, whereas variants expressing shorter allelic versions of each Vlp were susceptible. The target of growth-inhibiting Abs was not the Vlp products, since removal of anti-Vlp Abs had no effect on the inhibitory activity of the host immune serum on susceptible variants. Escape variant populations derived by propagating susceptible variants in an immune (versus control) host serum revealed a strong selection for the long-Vlp phenotype, irrespective of the identity of the Vlp expressed. Apparent mutational pathways of acquiring the protective phenotype included mutational switches to express long vlp genes that had been transcriptionally silent or switches to elongate expressed vlp genes. These results suggest that a major function of the Vlp system is to shield the wall-less mycoplasma surface from host Abs capable of binding vital (and as-yet-unidentified) surface antigens of this organism.
机译:根据其在确定生物体对宿主抗体(Abs)抑制生长的敏感性方面的作用,评估了支原体Vlp表面蛋白的变异。在猪肺炎支原体SK76的等基因谱系中已经研究了Vlp表面脂蛋白的高频转换。在这些谱系中,vlpA,vlpB和vlpC这三个基因的产物在体外会发生相位和大小变化,这是通过独立控制每个vlp基因表达(启动子突变)或大小的不同突变子发生的。 vlp基因产物(通过含有串联重复序列的3'区的基因内扩增或收缩)。评价了表达Vlp产物的不同概况的猪肺炎支原体SK76的同基因克隆变体对实验性感染了致关节炎性SK76菌株的猪的血清Abs对补体非依赖性生长抑制的敏感性。始终,表达较长版本的VlpA,VlpB或VlpC的变体(各自单独表达)对宿主免疫血清Ab完全耐药,而表达每个Vlp较短等位基因版本的变体易感。抑制生长的抗体的靶标不是Vlp产物,因为去除抗Vlp抗体对宿主免疫血清对易感变体的抑制活性没有影响。通过在免疫(相对于对照)宿主血清中繁殖易感变体而获得的逃逸变体种群显示出对长Vlp表型的强烈选择,而与所表达的Vlp的身份无关。获得保护性表型的明显突变途径包括表达长期沉默的长vlp基因的突变开关或延长表达的vlp基因的开关。这些结果表明,Vlp系统的主要功能是保护无壁支原体表面免受宿主Abs的侵害,该宿主Abs可以结合该生物的重要(至今尚未鉴定)表面抗原。

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