Identification of LukPQ, a novel, equid-adapted leukocidin of Staphylococcus aureus.
Identification of LukPQ, a novel, equid-adapted leukocidin of Staphylococcus aureus.
复制标题
LUKPQ的鉴定，这是金黄色葡萄球菌的新型，均等的白细胞素。
DOI：
10.1038/srep40660
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发表时间：
2017-01-20
影响因子：
4.6
通讯作者：
Holmes MA
中科院分区：
文献类型：
--
作者：
Koop G;Vrieling M;Storisteanu DM;Lok LS;Monie T;van Wigcheren G;Raisen C;Ba X;Gleadall N;Hadjirin N;Timmerman AJ;Wagenaar JA;Klunder HM;Fitzgerald JR;Zadoks R;Paterson GK;Torres C;Waller AS;Loeffler A;Loncaric I;Hoet AE;Bergström K;De Martino L;Pomba C;de Lencastre H;Ben Slama K;Gharsa H;Richardson EJ;Chilvers ER;de Haas C;van Kessel K;van Strijp JA;Harrison EM;Holmes MA
双组分成孔杀白素是由金黄色葡萄球菌分泌的一类强效毒素，主要针对白细胞，由S-和F-两种成分组成。S成分识别宿主细胞上的受体，实现与细胞表面的高亲和力结合，之后毒素形成穿透细胞脂质双层的毛孔。到目前为止，已经描述了六种不同的杀白素，其中一些是宿主和细胞特异性的。在这里，我们鉴定并鉴定了一种新的金黄色葡萄球菌杀白素：LukPQ。LukPQ编码在一个45 kb的原噬菌体(ΦSaeq1)上，在6个不同的克隆谱系中发现，几乎只存在于从马科动物培养的菌株中。我们证明LukPQ对马中性粒细胞具有强大而特异的杀伤作用，并确定马CXCRA和CXCR2为其靶向受体。虽然S组分(LukP)与LukED的S组分高度相似，但LukPQ和LukED的物种特异性不同。通过形成非规范的毒素对，我们发现F-组分对观察到的LukPQ的宿主趋向性有贡献，从而挑战了目前认为杀白素特异性完全由S-组分驱动的范式。
Bicomponent pore-forming leukocidins are a family of potent toxins secreted by Staphylococcus aureus, which target white blood cells preferentially and consist of an S- and an F-component. The S-component recognizes a receptor on the host cell, enabling high-affinity binding to the cell surface, after which the toxins form a pore that penetrates the cell lipid bilayer. Until now, six different leukocidins have been described, some of which are host and cell specific. Here, we identify and characterise a novel S. aureus leukocidin; LukPQ. LukPQ is encoded on a 45 kb prophage (ΦSaeq1) found in six different clonal lineages, almost exclusively in strains cultured from equids. We show that LukPQ is a potent and specific killer of equine neutrophils and identify equine-CXCRA and CXCR2 as its target receptors. Although the S-component (LukP) is highly similar to the S-component of LukED, the species specificity of LukPQ and LukED differs. By forming non-canonical toxin pairs, we identify that the F-component contributes to the observed host tropism of LukPQ, thereby challenging the current paradigm that leukocidin specificity is driven solely by the S-component.