neisseria meningitidis differentially controls host cell motility through pilc1 and pilc2 components of type iv pili脑膜炎奈瑟菌不同控制宿主细胞运动性通过pilc1和iv型菌毛的pilc2组件.pdfVIP

Neisseria meningitidis Differentially Controls Host Cell Motility through PilC1 and PilC2 Components of Type IV Pili Philippe C. Morand1,2,3*, Marek Drab1,4, Krishnaraj Rajalingam1¤, Xavier Nassif2,4, Thomas F. Meyer1 ´ ´ ´ 1 Department of Molecular Biology, Max-Planck-Institute for Infection Biology, Berlin, Germany, 2 Faculte de Medecine, Universite Paris Descartes, Paris, France, 3 INSERM ´ ´ ´ ´ (Institut National de la Sante et de la Recherche Medicale) U567, Institut Cochin, Paris, France, 4 INSERM (Institut National de la Sante et de la Recherche Medicale) U570, Paris, France Abstract Neisseria meningitidis is a strictly human pathogen that has two facets since asymptomatic carriage can unpredictably turn into fulminant forms of infection. Meningococcal pathogenesis relies on the ability of the bacteria to break host epithelial or endothelial cellular barriers. Highly restrictive, yet poorly understood, mechanisms allow meningococcal adhesion to cells of only human origin. Adhesion of encapsulated and virulent meningococci to human cells relies on the expression of bacterial type four pili (T4P) that trigger intense host cell signalling. Among the components of the meningococcal T4P, the concomitantly expressed PilC1 and PilC2 proteins regulate pili exposure at the bacterial surface, and until now, PilC1 was believed to be specifically responsible for T4P-mediated meningococcal adhesion to human cells. Contrary to previous reports, we show that, like PilC1, the meningococcal PilC2 component is capable of mediating adhesion to human ME180 epithelial cells, with cortical plaque formation and