EDIN-B在肺炎病程中促进金黄色葡萄球菌向血流的移位。
EDIN-B Promotes the Translocation of Staphylococcus aureus to the Bloodstream in the Course of Pneumonia.
作者信息
Courjon Johan, Munro Patrick, Benito Yvonne, Visvikis Orane, Bouchiat Coralie, Boyer Laurent, Doye Anne, Lepidi Hubert, Ghigo Eric, Lavigne Jean-Philippe, Vandenesch François, Lemichez Emmanuel
机构信息
INSERM U1065, Equipe Labellisée Ligue Contre le Cancer, Centre Méditerranéen de Médecine Moléculaire (C3M), Université de Nice Sophia-Antipolis, Nice 06204, France.
CIRI, International Center for Infectiology Research, Inserm U1111, Université Lyon 1, Ecole Normale Supérieure de Lyon, CNRS UMR5308, 7 Rue Guillaume Paradin, Lyon 69372, France.
出版信息
Toxins (Basel). 2015 Oct 15;7(10):4131-42. doi: 10.3390/toxins7104131.
It is crucial to define risk factors that contribute to host invasion by Staphylococcus aureus. Here, we demonstrate that the chromosomally encoded EDIN-B isoform from S. aureus contributes to the onset of bacteremia during the course of pneumonia. Deletion of edinB in a European lineage community-acquired methicillin resistant S. aureus (CA-MRSA) strain (ST80-MRSA-IV) dramatically decreased the frequency and magnitude of bacteremia in mice suffering from pneumonia. This deletion had no effect on the bacterial burden in both blood circulation and lung tissues. Re-expression of wild-type EDIN-B, unlike the catalytically inactive mutant EDIN-R185E, restored the invasive characteristics of ST80-MRSA-IV.
确定导致金黄色葡萄球菌侵袭宿主的风险因素至关重要。在此，我们证明来自金黄色葡萄球菌的染色体编码EDIN - B异构体在肺炎病程中促成菌血症的发生。在一株欧洲谱系社区获得性耐甲氧西林金黄色葡萄球菌（CA - MRSA）菌株（ST80 - MRSA - IV）中删除edinB，显著降低了患肺炎小鼠菌血症的频率和程度。这种缺失对血液循环和肺组织中的细菌载量没有影响。与催化无活性的突变体EDIN - R185E不同，野生型EDIN - B的重新表达恢复了ST80 - MRSA - IV的侵袭特性。
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