The genus Neisseria includes many commensal species that form part of the flora of human and animal mucosa, but also includes two major pathogenic species: N. gonorrhoeae and N. meningitidis inhabits the upper respiratory tract and can cause meningococcal disease, a disease of rapid onset that involves sepsis and meningitis. N. gonorrhoeae lives in the genital, rectal, and oral mucosa, and can cause gonorrhoeal infection that involves pelvic inflammatory disease, infertility, and ectopic pregnancy. Additionally, it can cause neonatal blindness when transferred from an infected mother to the neonate during delivery.
To cause disease, both Neisseria species utilize a range of virulence factors that evade and suppress the natural and adaptive immune response. Neisseria virulence factors include a repertoire of surface exposed structures that are secreted by multiple secretion systems, including type I and type V. Examples are capsule, autotransporters, lipoproteins, pili, extracellular proteins, or even integral membrane proteins. Many of these are combined with many immune evasion mechanisms, such as antigenic variation and phase variable protein production. In addition, both bacteria species can form biofilms - bacterial associations that help to evade the immune system and resist environment aggressions.
Over the last two decades, N. meningitidis vaccine research has attracted much attention, particularly due to the high incidence of meningococcal disease, and the difficulties in obtaining a vaccine against isolates producing the serogroup B capsule. The intensive research resulted in commercial vaccines based on subcapsular antigens. In contrast, N. gonorrhoeae vaccine research is still ongoing, some of the blockers for this includes the difficulties in generating host protection at the particular gonococcal niches, and the high number of mechanisms used by this pathogen to escape the adaptive immune response.
The lack of a vaccine formula to stop gonococcus colonization and infection is accompanied by increasing worldwide gonococcus infections and the isolation of many multidrug resistant bacteria. Indeed, N. gonorrhoeae has an extraordinary capacity to escape antibiotic activities through many mechanisms such as regulation of the traffic of antibiotics, production of antibiotic degrading enzymes, or the alteration of antibiotic targets. Moreover, the high capacity of this microorganism to rapidly generate biofilms contribute to antibiotic tolerance by mechanism such as retaining antibiotics in the biofilm matrix, reduction of the access of antibiotics to biofilm members, or physiological and phenotypic changes that affect antibiotic effectivity, among others.
The goal of this Research Topic is therefore to gain insides in new virulent factors, including proteins and lipids with a role in virulence and novel functions and mechanisms of already known structures with a role in virulence of these pathogens. With this aim, we intend to welcome novel findings on how surface structures facilitate and modulate the pathogenesis. Additionally, we intend to understand antibiotic resistance and antibiotic tolerance mechanisms in Neisseria, including gene mutations in antibiotic targets, mechanism of antibiotic uptake and novel genes involved in antibiotic resistance. It will be also of interest how bacteria persist antibiotics by biofilm formation.
We welcome submissions of original research articles, reviews, and mini reviews on but not limited to the following subthemes on the pathogenesis of Neisseria species:
• The elucidation of mechanisms, including regulation, interaction networks, signalling pathways, phenotypes or on the interaction between the pathogen and the host.
• Studies on proteomic, lipidomics, and transcriptomic analysis that highlight or bring out a signature molecule are also welcome.
• The characterization of pathogenic Neisseria virulence factors including molecular mechanisms.
• Neisseria mechanisms of biofilm formation.
• N. gonorrhoeae and N. meningitidis antibiotic resistance and tolerance.
• Vaccinology as well as novel substances with bactericidal effect on pathogenic Neisseria with the potential to contribute as future alternatives to antibiotics.
The genus Neisseria includes many commensal species that form part of the flora of human and animal mucosa, but also includes two major pathogenic species: N. gonorrhoeae and N. meningitidis inhabits the upper respiratory tract and can cause meningococcal disease, a disease of rapid onset that involves sepsis and meningitis. N. gonorrhoeae lives in the genital, rectal, and oral mucosa, and can cause gonorrhoeal infection that involves pelvic inflammatory disease, infertility, and ectopic pregnancy. Additionally, it can cause neonatal blindness when transferred from an infected mother to the neonate during delivery.
To cause disease, both Neisseria species utilize a range of virulence factors that evade and suppress the natural and adaptive immune response. Neisseria virulence factors include a repertoire of surface exposed structures that are secreted by multiple secretion systems, including type I and type V. Examples are capsule, autotransporters, lipoproteins, pili, extracellular proteins, or even integral membrane proteins. Many of these are combined with many immune evasion mechanisms, such as antigenic variation and phase variable protein production. In addition, both bacteria species can form biofilms - bacterial associations that help to evade the immune system and resist environment aggressions.
Over the last two decades, N. meningitidis vaccine research has attracted much attention, particularly due to the high incidence of meningococcal disease, and the difficulties in obtaining a vaccine against isolates producing the serogroup B capsule. The intensive research resulted in commercial vaccines based on subcapsular antigens. In contrast, N. gonorrhoeae vaccine research is still ongoing, some of the blockers for this includes the difficulties in generating host protection at the particular gonococcal niches, and the high number of mechanisms used by this pathogen to escape the adaptive immune response.
The lack of a vaccine formula to stop gonococcus colonization and infection is accompanied by increasing worldwide gonococcus infections and the isolation of many multidrug resistant bacteria. Indeed, N. gonorrhoeae has an extraordinary capacity to escape antibiotic activities through many mechanisms such as regulation of the traffic of antibiotics, production of antibiotic degrading enzymes, or the alteration of antibiotic targets. Moreover, the high capacity of this microorganism to rapidly generate biofilms contribute to antibiotic tolerance by mechanism such as retaining antibiotics in the biofilm matrix, reduction of the access of antibiotics to biofilm members, or physiological and phenotypic changes that affect antibiotic effectivity, among others.
The goal of this Research Topic is therefore to gain insides in new virulent factors, including proteins and lipids with a role in virulence and novel functions and mechanisms of already known structures with a role in virulence of these pathogens. With this aim, we intend to welcome novel findings on how surface structures facilitate and modulate the pathogenesis. Additionally, we intend to understand antibiotic resistance and antibiotic tolerance mechanisms in Neisseria, including gene mutations in antibiotic targets, mechanism of antibiotic uptake and novel genes involved in antibiotic resistance. It will be also of interest how bacteria persist antibiotics by biofilm formation.
We welcome submissions of original research articles, reviews, and mini reviews on but not limited to the following subthemes on the pathogenesis of Neisseria species:
• The elucidation of mechanisms, including regulation, interaction networks, signalling pathways, phenotypes or on the interaction between the pathogen and the host.
• Studies on proteomic, lipidomics, and transcriptomic analysis that highlight or bring out a signature molecule are also welcome.
• The characterization of pathogenic Neisseria virulence factors including molecular mechanisms.
• Neisseria mechanisms of biofilm formation.
• N. gonorrhoeae and N. meningitidis antibiotic resistance and tolerance.
• Vaccinology as well as novel substances with bactericidal effect on pathogenic Neisseria with the potential to contribute as future alternatives to antibiotics.
