A Case for the Evolution from Commensalism to Pathogenicity and Possibly Back Again: Lessons Learned from the Human-Adapted Neisseria Species

Priniski, Lauren L.; Seifert, H. Steven

doi:10.1007/978-3-319-69078-0_13

Cited by 3 publications

(4 citation statements)

References 243 publications

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“…Interestingly, the acquisition of these responses is suggested as a defining event in the evolution of the commensals, Neisseria lactamica and Neisseria polysaccharea. These commensals are hypothesized to have evolved from the pathogenic Neisseria species, suggesting an evolutionary route from commensalism, to pathogenicity, and back to commensalism (Priniski and Seifert, 2018).…”

Section: Discussionmentioning

confidence: 99%

Mechanisms of host manipulation by Neisseria gonorrhoeae

et al. 2023

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Neisseria gonorrhoeae (also known as gonococcus) has been causing gonorrhoea in humans since ancient Egyptian times. Today, global gonorrhoea infections are rising at an alarming rate, in concert with an increasing number of antimicrobial-resistant strains. The gonococcus has concurrently evolved several intricate mechanisms that promote pathogenesis by evading both host immunity and defeating common therapeutic interventions. Central to these adaptations is the ability of the gonococcus to manipulate various host microenvironments upon infection. For example, the gonococcus can survive within neutrophils through direct regulation of both the oxidative burst response and maturation of the phagosome; a concerning trait given the important role neutrophils have in defending against invading pathogens. Hence, a detailed understanding of how N. gonorrhoeae exploits the human host to establish and maintain infection is crucial for combating this pathogen. This review summarizes the mechanisms behind host manipulation, with a central focus on the exploitation of host epithelial cell signaling to promote colonization and invasion of the epithelial lining, the modulation of the host immune response to evade both innate and adaptive defenses, and the manipulation of host cell death pathways to both assist colonization and combat antimicrobial activities of innate immune cells. Collectively, these pathways act in concert to enable N. gonorrhoeae to colonize and invade a wide array of host tissues, both establishing and disseminating gonococcal infection.

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Section: Discussionmentioning

confidence: 99%

Mechanisms of host manipulation by Neisseria gonorrhoeae

et al. 2023

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“…The genus Neisseria contains many species of environmental, mammalian and reptilian origin [60], and it has been hypothesized that a transition to humans occurred in the distant past. Priniski and Seifert [61] presented a model in which they hypothesized that an early ancestor evolved into all 11 of the obligate human colonizing Neisseria spcies. Vazquez et al [62] had advanced an earlier model implying that N. meningitidis and N. gonorrhoeae share a common ancestor and recent work from Vigue and Eyre-Walker [63] substantiated this further, showing evidence that both species have diverged through adaptive evolution propelled by lateral gene transfer.…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Modelling evolutionary pathways for commensalism and hypervirulence in Neisseria meningitidis

et al. 2021

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Neisseria meningitidis , the meningococcus, resides exclusively in humans and causes invasive meningococcal disease (IMD). The population of N. meningitidis is structured into stable clonal complexes by limited horizontal recombination in this naturally transformable species. N. meningitidis is an opportunistic pathogen, with some clonal complexes, such as cc53, effectively acting as commensal colonizers, while other genetic lineages, such as cc11, are rarely colonizers but are over-represented in IMD and are termed hypervirulent. This study examined theoretical evolutionary pathways for pathogenic and commensal lineages by examining the prevalence of horizontally acquired genomic islands (GIs) and loss-of-function (LOF) mutations. Using a collection of 4850 genomes from the BIGSdb database, we identified 82 GIs in the pan-genome of 11 lineages (10 hypervirulent and one commensal lineage). A new computational tool, Phaser, was used to identify frameshift mutations, which were examined for statistically significant association with genetic lineage. Phaser identified a total of 144 frameshift loci of which 105 were shown to have a statistically significant non-random distribution in phase status. The 82 GIs, but not the LOF loci, were associated with genetic lineage and invasiveness using the disease carriage ratio metric. These observations have been integrated into a new model that infers the early events of the evolution of the human adapted meningococcus. These pathways are enriched for GIs that are involved in modulating attachment to the host, growth rate, iron uptake and toxin expression which are proposed to increase competition within the meningococcal population for the limited environmental niche of the human nasopharynx. We surmise that competition for the host mucosal surface with the nasopharyngeal microbiome has led to the selection of isolates with traits that enable access to cell types (non-phagocytic and phagocytic) in the submucosal tissues leading to an increased risk for IMD.

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“…Av is a common process in many microbial pathogens, including viruses and bacteria, and eukaryotic parasites (1–4). Gene diversification allows for stochastic population heterogeneity, which can be beneficial at the population level when selection occurs (5). While the name suggest that these systems are in response to immune surveillance, the variation can be useful for both immune and other function selection on the population level.…”

Section: Introductionmentioning

confidence: 99%

PacBio Amplicon Sequencing Method To Measure Pilin Antigenic Variation Frequencies of Neisseria gonorrhoeae

Ozer

Prister

Yin

et al. 2019

mSphere

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Gene diversification is a common mechanism pathogens use to alter surface structures to aid in immune avoidance. Neisseria gonorrhoeae uses a gene conversion-based diversification system to alter the primary sequence of the gene encoding the major subunit of the pilus, pilE. Antigenic variation occurs when one of the nonexpressed 19 silent copies donates part of its DNA sequence to pilE. We have developed a method using Pacific Biosciences (PacBio) amplicon sequencing and custom software to determine pilin antigenic variation frequencies. The program analyzes 37 variable regions across the strain FA1090 1-81-S2 pilE gene and can be modified to determine sequence variation from other starting pilE sequences or other diversity generation systems. Using this method, we measured pilin antigenic variation frequencies for various derivatives of strain FA1090 and showed we can also analyze pilin antigenic variation frequencies during macrophage infection. IMPORTANCE Diversity generation systems are used by many unicellular organism to provide subpopulations of cell with different properties that are available when needed. We have developed a method using the PacBio DNA sequencing technology and a custom computer program to analyze the pilin antigenic variation system of the organism that is the sole cause of the sexually transmitted infection, gonorrhea.

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A Case for the Evolution from Commensalism to Pathogenicity and Possibly Back Again: Lessons Learned from the Human-Adapted Neisseria Species

Cited by 3 publications

References 243 publications

Mechanisms of host manipulation by Neisseria gonorrhoeae

Mechanisms of host manipulation by Neisseria gonorrhoeae

Modelling evolutionary pathways for commensalism and hypervirulence in Neisseria meningitidis

PacBio Amplicon Sequencing Method To Measure Pilin Antigenic Variation Frequencies of Neisseria gonorrhoeae

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