About: Colonization of the murine oropharynx by Streptococcus pyogenes is governed by the Rgg2/3 quorum sensing system

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About: Colonization of the murine oropharynx by Streptococcus pyogenes is governed by the Rgg2/3 quorum sensing system Goto Sponge NotDistinct Permalink

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
title	Colonization of the murine oropharynx by Streptococcus pyogenes is governed by the Rgg2/3 quorum sensing system
Creator	Federle, Michael Gogos, Artemis
source	BioRxiv
abstract	Streptococcus pyogenes is a human-restricted pathogen most often found in the human nasopharynx. Multiple bacterial factors are known to contribute to persistent colonization of this niche, and many are important in mucosal immunity and vaccine development. In this work, mice were infected intranasally with transcriptional regulator mutants of the Rgg2/3 quorum sensing (QS) system—a peptide-based signaling system conserved in sequenced isolates of S. pyogenes. Deletion of the QS system’s transcriptional activator (Δrgg2) dramatically diminished the percentage of colonized mice while deletion of the transcriptional repressor (Δrgg3) increased the percentage of colonized mice compared to wild type. Stimulation of the QS system using synthetic pheromones prior to inoculation did not significantly increase the percentage of animals colonized, indicating that QS-dependent colonization is responsive to the intrinsic conditions within the host upper respiratory tract. Bacterial RNA extracted directly from oropharyngeal swabs and evaluated by quantitative RT-PCR subsequently confirmed QS upregulation within one hour of inoculation. In the nasal-associated lymphoid tissue (NALT), a muted inflammatory response to the Δrgg2 bacteria suggests that their rapid elimination failed to elicit the previously characterized response to intranasal inoculation of GAS. This work identifies a new transcriptional regulatory system governing the ability of S. pyogenes to colonize the nasopharynx and provides knowledge that could help lead to decolonization therapeutics. Author Summary Streptococcus pyogenes is responsible for a wide spectrum of diseases ranging from common pharyngitis to infrequent invasive infections like necrotizing fasciitis. The ability of this microorganism to persist in the human oropharynx predisposes colonized individuals to a variety of superficial and invasive diseases which lead to significant morbidities and mortality. Identification of the regulatory systems that augment the bacteria’s ability to colonize the oropharynx provides potential targets against which molecular therapeutics can be designed. Here we show that the Rgg2/3 quorum sensing system, an interbacterial communication system, governs the ability of S. pyogenes to colonize the murine oropharynx. Disruption of the system’s transcriptional activator reduced colonization dramatically, eliminated the transcription of two sets of genes known to be activated by the Rgg2/3 system, and tempered the innate immune response seen when S. pyogenes is intranasally infected into the mouse.
has issue date	2020-06-30(xsd:dateTime)
bibo:doi	10.1101/2020.06.30.179903
has license	biorxiv
sha1sum (hex)	52c7cbd95c3c7a6c2a92d36c89f4de33986684cd
schema:url	https://doi.org/10.1101/2020.06.30.179903
resource representing a document's title	Colonization of the murine oropharynx by Streptococcus pyogenes is governed by the Rgg2/3 quorum sensing system
schema:publication	bioRxiv
resource representing a document's body	covid:52c7cbd95c3c7a6c2a92d36c89f4de33986684cd#body_text
is schema:about of	named entity 'Streptococcus pyogenes' named entity 'GAS' named entity 'immune response' named entity 'RNA' named entity 'CXCL9' »more»

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