The CRISPR/Cas system in <i>Neisseria meningitidis</i> affects bacterial adhesion to human nasopharyngeal epithelial cells

<i>Neisseria meningitidis</i>, a commensal β-proteobacterium of the human nasopharynx, constitutes a worldwide leading cause of sepsis and epidemic meningitis. A recent genome-wide association study suggested an association of its type II-C CRISPR/Cas system with carriage and thus less invasive lineages. Here, we show that knock-out strains lacking the Cas9 protein are impaired in the adhesion to human nasopharyngeal cells which constitutes a central step in the pathogenesis of invasive meningococcal disease. Transcriptome sequencing data further suggest that meningococcal Cas9 does not affect the expression of surface adhesins but rather exerts its effect on cell adhesion in an indirect manner. Consequently, we speculate that the meningococcal CRISPR/Cas system exerts novel functions beyond its established role in defence against foreign DNA.

脑膜炎奈瑟菌（Neisseria meningitidis）是寄居于人类鼻咽部的共生β-变形菌，是全球范围内引发败血症与流行性脑膜炎的首要致病菌。近期一项全基因组关联研究表明，其II-C型CRISPR/Cas系统与带菌状态（即低侵袭性谱系）存在关联。本研究显示，缺失Cas9蛋白的敲除菌株在黏附人类鼻咽细胞的能力上存在缺陷，而该黏附过程是侵袭性脑膜炎球菌疾病发病机制中的核心步骤。转录组测序数据进一步表明，脑膜炎球菌Cas9并不会影响表面黏附素的表达，而是以间接方式对细胞黏附发挥调控作用。据此我们推测，脑膜炎球菌CRISPR/Cas系统除了其既定的抵御外源DNA的功能外，还具备全新的生物学功能。