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首页> 外文期刊>Infection and immunity >Mutation of the Maturase Lipoprotein Attenuates the Virulence of Streptococcus equi to a Greater Extent than Does Loss of General Lipoprotein Lipidation
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Mutation of the Maturase Lipoprotein Attenuates the Virulence of Streptococcus equi to a Greater Extent than Does Loss of General Lipoprotein Lipidation

机译：成熟酶脂蛋白的突变比普通脂蛋白脂化的损失更能减弱马链球菌的毒性。

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Streptococcus equi is the causative agent of strangles, a prevalent and highly contagious disease of horses. Despite the animal suffering and economic burden associated with strangles, little is known about the molecular basis of S. equi virulence. Here we have investigated the contributions of a specific lipoprotein and the general lipoprotein processing pathway to the abilities of S. equi to colonize equine epithelial tissues in vitro and to cause disease in both a mouse model and the natural host in vivo. Colonization of air interface organ cultures after they were inoculated with a mutant strain deficient in the maturase lipoprotein (ΔprtM138-213, with a deletion of nucleotides 138 to 213) was significantly less than that for cultures infected with wild-type S. equi strain 4047 or a mutant strain that was unable to lipidate preprolipoproteins (Δlgt190-685). Moreover, mucus production was significantly greater in both wild-type-infected and Δlgt190-685-infected organ cultures. Both mutants were significantly attenuated compared with the wild-type strain in a mouse model of strangles, although 2 of 30 mice infected with the Δlgt190-685 mutant did still exhibit signs of disease. In contrast, only the ΔprtM138-213 mutant was significantly attenuated in a pony infection study, with 0 of 5 infected ponies exhibiting pathological signs of strangles compared with 4 of 4 infected with the wild-type and 3 of 5 infected with the Δlgt190-685 mutant. We believe that this is the first study to evaluate the contribution of lipoproteins to the virulence of a gram-positive pathogen in its natural host. These data suggest that the PrtM lipoprotein is a potential vaccine candidate, and further investigation of its activity and its substrate(s) are warranted.
机译：链球菌是勒死的病原体，勒死是马的一种普遍且高度传染的疾病。尽管勒死动物带来痛苦和经济负担，但对 S的分子基础知之甚少。等毒力。在这里，我们研究了特定脂蛋白和一般脂蛋白加工途径对 S能力的贡献。 equi 在体外定植马上皮组织，并在小鼠模型和体内天然宿主中引起疾病​​。接种缺乏成熟酶脂蛋白的突变菌株（Δ prtM 138 - 213 < / sub>，其核苷酸138至213的缺失显着小于野生型 S感染的培养物。 equi 菌株4047或无法脂化前脂蛋白的突变株（Δ lgt 190 - 685 ）。而且，野生型和Δ lgt 190 - 685 感染的粘液产生均显着增加器官文化。在勒死的小鼠模型中，与野生型菌株相比，这两种突变体均显着减毒，尽管在感染Δ lgt 190 -的30只小鼠中有2只sub> 685 突变体仍显示出疾病迹象。相比之下，在小马感染研究中，只有Δ prtM 138 - 213 突变体显着减弱，0 5个受感染的小马表现出勒死的病理征兆，而野生型感染的4个小马中有4个感染了Δ lgt 190 -的5个中有3个sub> 685 突变体。我们相信这是第一项评估脂蛋白对自然宿主中革兰氏阳性病原体毒力的贡献的研究。这些数据表明PrtM脂蛋白是潜在的疫苗候选物，因此有必要对其活性及其底物​​进行进一步研究。

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