The Biology of Neisseria Adhesins

Abstract

Members of the genus Neisseria include pathogens causing important human diseases such as meningitis, septicaemia, gonorrhoea and pelvic inflammatory disease syndrome. Neisseriae are found on the exposed epithelia of the upper respiratory tract and the urogenital tract. Colonisation of these exposed epithelia is dependent on a repertoire of diverse bacterial molecules, extending not only from the surface of the bacteria but also found within the outer membrane. During invasive disease, pathogenic Neisseriae also interact with immune effector cells, vascular endothelia and the meninges. Neisseria adhesion involves the interplay of these multiple surface factors and in this review we discuss the structure and function of these important molecules and the nature of the host cell receptors and mechanisms involved in their recognition. We also describe the current status for recently identified Neisseria adhesins. Understanding the biology of Neisseria adhesins has an impact not only on the development of new vaccines but also in revealing fundamental knowledge about human biology.

Inhibitors of the Neisseria meningitidis PilF ATPase provoke type IV pilus disassembly

“…We chose this phenotypic approach because it has the potential to reveal active compounds while remaining agnostic on the potential targets involved in bacterial adhesion. Converging with previous studies identifying the role of meningococcal Tfp in the interaction with endothelial cells (11,13), we discovered compounds that inhibit type IV pili assembly. Because of the importance of this virulence factor in vivo (13), these compounds represent attractive candidates for adjuvant therapy in combination with existing antibiotics.…”

“…Central virulent properties of N. meningitidis include adhesion to host cells (11), and this constitutes an original and attractive target for treatments. Adhesion of N. meningitidis to human cells is a key step in the life cycle of this organism by allowing nasopharynx colonization and adhesion to endothelial cells, each of these events promoting blood and brain colonization by the bacteria.…”

Large scale genomic analysis shows no evidence for repeated pathogen adaptation during the invasive phase of bacterial meningitis in humans

“…Some of the mutations upstream of porA and opc are in phase variable homopolymeric tracts, which are discussed more fully in the section below. The other mutations are upstream of the adhesins hsf /NMB0992 and NMB1994, which are involved in colonisation [53] and immune interaction during invasion [54], and frpB /NMB1988 which is a surface antigen involved in iron uptake [55]. Differential expression of these genes may be an important factor affecting invasion, but the mutations we observed that may affect this do not appear to be specific to blood or CSF.…”

Alterations and correlations of the gut microbiome, metabolism and immunity in patients with primary biliary cirrhosis

“…Consistent with this conclusion, increases in liver injury indicators, serum inflammatory cytokines, or disorders of tryptophan metabolism are positively associated with enrichments of the above opportunistic pathogens in PBC patients, such as the intensive association of Klebsiella bacteria with IL‐2RA, GRO‐α and MIF; Megasphaera micronuciformis with IL‐18; Anaeroglobus geminatus with the Mayo risk score; Enterobacter asburiae with IL‐18 and SCF; Paraprevotella clara with total protein and globulin; and the Neisseriaceae bacteria and Klebsiella bacteria with urinary indoleacrylate. As reported, Actinobacillus pleuropneumoniae is a major cause of respiratory disease in pigs (Klinkenberg et al ., ); Enterobacter asburiae is an opportunistic pathogen related to community‐acquired pneumonia, soft tissue infections and wound infection (Mardaneh and Soltan Dallal, ); ankylosing spondylitis and Crohn's disease are likely caused by subclinical bowel infections with Klebsiella microbes (Rashid and Ebringer, ; Sung et al ., ); and several members of Neisseria are pathogens that cause important diseases (Hung and Christodoulides, ).…”