Abstract
It is now abundantly clear that our microbiota (commensals) are critical for many physiological and developmental processes. They have also been shown to inhibit pathogen colonization, through a variety of means including nutrient competition and secretion of microbicidal or biofilm-inhibiting proteins/peptides. Our recent study, Kim et al., (2019), adds a new dimension to the concept of commensal protection. It shows that commensal Neisseria kill the closely related pathogen N. gonorrhoeae through an unexpected mechanism, one that involves genetic competence, DNA methylation state and recombination. This microreview summarizes the report and discusses questions and lines of research arising from the study. Further investigation into this DNA-based killing mechanism will provide a better understanding of Neisseria biology and commensal-pathogen interactions on the mucosa, and identify strategies for preventing pathogenic Neisseria transmission.
Highlights
GENESIS OF THE STUDY The Gram negative Neisseria genus contains many species that naturally colonize a wide range of animals, including man
COMMENSAL NEISSERIA KILL PATHOGENIC NEISSERIA VIA ITS DNA We found that Neisseria gonorrhoeae (Ngo) is killed in the presence of the human commensal Neisseria elongata (Nel), and the toxic compound is Nel DNA that accumulated in the medium
As commensal DNA altered to mimic the Ngo methylation pattern is less toxic to Ngo, we propose that Ngo restriction enzyme(s) cleave at cognate sequences in these heteroduplexes
Summary
GENESIS OF THE STUDY The Gram negative Neisseria genus contains many species that naturally colonize a wide range of animals, including man. Tribal warfare: Commensal Neisseria kill pathogen Neisseria gonorrhoeae using its DNA * Corresponding Author: Magdalene So, Department of Immunobiology and the BIO5 Institute, University of Arizona, Tucson, AZ 85721, USA; E-mail: somaggie@email.arizona.edu It shows that commensal Neisseria kill the closely related pathogen N. gonorrhoeae through an unexpected mechanism, one that involves genetic competence, DNA methylation state and recombination.
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