Commensal Neisseria Kill Neisseria gonorrhoeae through a DNA-Dependent Mechanism.
DNA killing of pathogens
DNA uptake
commensal Neisseria
pathogenic Neisseria
Journal
Cell host & microbe
ISSN: 1934-6069
Titre abrégé: Cell Host Microbe
Pays: United States
ID NLM: 101302316
Informations de publication
Date de publication:
14 08 2019
14 08 2019
Historique:
received:
23
01
2019
revised:
25
04
2019
accepted:
11
07
2019
pubmed:
6
8
2019
medline:
20
12
2019
entrez:
6
8
2019
Statut:
ppublish
Résumé
The mucosa is colonized with commensal Neisseria. Some of these niches are sites of infection for the STD pathogen Neisseria gonorrhoeae (Ngo). Given the antagonistic behavior of commensal bacteria toward their pathogenic relatives, we hypothesized that commensal Neisseria may negatively affect Ngo colonization. Here, we report that commensal species of Neisseria kill Ngo through a mechanism based on genetic competence and DNA methylation state. Specifically, commensal-triggered killing occurs when the pathogen takes up commensal DNA containing a methylation pattern that it does not recognize. Indeed, any DNA will kill Ngo if it can enter the cell, is differentially methylated, and has homology to the pathogen genome. Consistent with these findings, commensal Neisseria elongata accelerates Ngo clearance from the mouse in a DNA-uptake-dependent manner. Collectively, we propose that commensal Neisseria antagonizes Ngo infection through a DNA-mediated mechanism and that DNA is a potential microbicide against this highly drug-resistant pathogen.
Identifiants
pubmed: 31378677
pii: S1931-3128(19)30347-6
doi: 10.1016/j.chom.2019.07.003
pmc: PMC6728082
mid: NIHMS1535495
pii:
doi:
Substances chimiques
DNA, Bacterial
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
228-239.e8Subventions
Organisme : NIAID NIH HHS
ID : R21 AI111944
Pays : United States
Commentaires et corrections
Type : CommentIn
Type : CommentIn
Type : CommentIn
Informations de copyright
Copyright © 2019 Elsevier Inc. All rights reserved.
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