Meningococcal Ligands and Molecular Targets of the Host
Meningococcal mechanisms of adhesion are complex, involving multiple adhesins and their respective target receptors on host cells. Three major surface structures – pili, Opa, and Opc – have been known for some time to mediate meningococcal adhesion to tar
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ion The last two decades have seen a considerable advancement in our understanding of the complexities of Neisseria meningitidis (meningococcus) pathogenic mechanisms. The research has been fuelled by developments in the areas of genomics, transcriptomics, and proteomics. Such advances have improved our understanding of how meningococci alter their metabolism in response to different
Myron Christodoulides (ed.), Neisseria meningitidis: Advanced Methods and Protocols, Methods in Molecular Biology, vol. 799, DOI 10.1007/978-1-61779-346-2_9, © Springer Science+Business Media, LLC 2012
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D.J. Hill and M. Virji
environments, acquire factors such as iron, as well as alter the array of surface molecules, which can be frequent and complex. Our understanding of how such molecules interact with host components promoting adhesion and influencing the immune response has also been enhanced by such studies. However, while many new surface molecules of the pathogen have been revealed by genome sequencing and mining, their functions remain to be fully defined. Indeed, the molecular mechanisms of even the traditional and long-known major adhesins are still unclear and some of their host cell targets remain undefined. This compendium provides background on meningococcal adhesins and their (putative) receptors as a prelude to the following chapters that describe some of the approaches used in studying pathogen–host cell interactions.
2. Meningococcal Adhesins and Cell Surface Located Human Receptors
2.1. Pili and Their Putative Receptors
Meningococcal adhesins can be divided into three broad structural classes, the polymeric hair-like pili, the integral outer membrane proteins (OMP), including the opacity proteins Opa and Opc, which are usually beta barrel structures, and the autotransporters (including meningococcal serine protease (Msp)A), meningococcal surface fibril (Msf, or Neisseria hia homolog (Nhh)A), and Neisseria adhesin (Nad)A, which have only recently emerged as significant contenders as adhesins. In addition, surface carbohydrates can be classified as adhesins as well as anti-adhesins as they can interfere with integral OMP function. Further, enzymes and envelopeassociated proteins have also been postulated to be involved in cellular interaction of meningococci (Table 1). This compendium focuses principally on bacterial structures supporting adhesion to host cells. It should be noted that the following chapters also provide details of host receptors and cells involved in host immune function such as pattern recognition receptors and dendritic cells. Whilst several meningococcal adhesins have now been described, information on receptors utilised by them is often lacking. However, key methods such as receptor overlay of western blots containing bacterial proteins or vice versa (Far-Western blotting) and coprecipitation in combination with techniques to visualise and/or quantify bacterial adhesion (immunofluorescence microscopy, viable count assays) has led to the identification of cognate receptors for some of the nei
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