Location, Location, Location—Commensalism, Damage and Evolution of the Pathogenic Neisseria

The 10 human-restricted Neisseria species all colonize mucosal surfaces, but show a spectrum of pathogenicity. The commensal Neisseria do not normally cause pathology, while the two pathogenic species, Neisseria meningitidis and Neisseria gonorrhoeae, straddle the border between commensalism and pat...

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Bibliographic Details
Published in:Journal of molecular biology 2019-07, Vol.431 (16), p.3010-3014
Main Author: Seifert, H Steven
Format: Article
Language:English
Subjects:
bacterial meningitis
commensalism
evolution
gonorrhea
polymorphonuclear leukocytes
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Summary:The 10 human-restricted Neisseria species all colonize mucosal surfaces, but show a spectrum of pathogenicity. The commensal Neisseria do not normally cause pathology, while the two pathogenic species, Neisseria meningitidis and Neisseria gonorrhoeae, straddle the border between commensalism and pathogenicity. Why the pathogenic Neisseria continue to mediate host damage after thousands of years of co-evolution with their human host, and why the commensal species have not acquired the ability to damage the host, if this capability provides a selective advantage, is not understood. One way the pathogenic species are different from the commensal species is by their ability to induce PMN inflammation, which is dependent on the site of colonization. I discuss how the site of colonization dictates whether copious inflammation occurs with both pathogenic species. I put forth a model that posits that an ancestor of both pathogenic species changed colonization site from the oral cavity to the genital tract of a human or humanoid and had to evolve multiple, new traits — to induce PMN inflammation and avoid adaptive immunity — to allow efficient sexual transmission. This model predicts that PMN inflammation produces the serious sequelae of gonorrhea and increases the probability that N. meningitidis might exit the oral cavity to produce systemic disease. In both cases, the pathology produced by these host-adapted species is an unintended by product of the inflammation but host damage does not provide any selective advantage for these organisms. [Display omitted] •There are several human-restricted Neisseria species that show a gradient of pathogenicity.•The commensal Neisseria rarely cause damage to the host. Neisseria meningiditis only causes morbidity and mortality when it leaves the nasal pharynx. Neisseria gonorrhoeae more readily induces polymorphonuclear leukocyte (PMN) inflammation and colonization of alternate anatomical sites results in host damage.•In contrast to the other Neisseria, colonization of N. gonorrhea that does not elicit symptoms is classified as asymptomatic infection rather than commensal colonization.•The level of PMN inflammation is influenced by the Neisseria species involved and the site of colonization. Whether PMNs are always recruited during the colonization of different sites is not known.•The two pathogenic Neisseria arose from a common ancestor.•A model for the evolution of the pathogenic species is proposed where a common, progenito
ISSN:0022-2836
1089-8638
DOI:10.1016/j.jmb.2019.04.007