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dc.contributor.authorChaudhuri, Swarnava
dc.contributor.authorGantner, Benjamin N.
dc.contributor.authorYe, Richard D.
dc.contributor.authorCianciotto, Nicholas P.
dc.contributor.authorFreitag, Nancy E.
dc.date.accessioned2013-10-22T22:01:20Z
dc.date.available2013-10-22T22:01:20Z
dc.date.issued2013-03
dc.identifier.bibliographicCitationChaudhuri S, Gantner BN, Ye RD, Cianciotto NP, Freitag NE. 2013. The Listeria monocytogenes ChiA chitinase enhances virulence through suppression of host innate immunity. mBio 4(2):e00617-12. doi:10.1128/mBio.00617-12.en_US
dc.identifier.issn2150-7511
dc.identifier.urihttp://hdl.handle.net/10027/10110
dc.description© 2013 Chaudhuri et al. This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-ShareAlike 3.0 Unported license, which permits unrestricted noncommercial use, distribution, and reproduction in any medium, provided the original author and source are credited.en_US
dc.description.abstractEnvironmental pathogens survive and replicate within the outside environment while maintaining the capacity to infect mammalian hosts. For some microorganisms, mammalian infection may be a relatively rare event. Understanding how environmental pathogens retain their ability to cause disease may provide insight into environmental reservoirs of disease and emerging infections. Listeria monocytogenes survives as a saprophyte in soil but is capable of causing serious invasive disease in susceptible individuals. The bacterium secretes virulence factors that promote cell invasion, bacterial replication, and cell-to-cell spread. Recently, an L. monocytogenes chitinase (ChiA) was shown to enhance bacterial infection in mice. Given that mammals do not synthesize chitin, the function of ChiA within infected animals was not clear. Here we have demonstrated that ChiA enhances L. monocytogenes survival in vivo through the suppression of host innate immunity. L. monocytogenes Delta chiA mutants were fully capable of establishing bacterial replication within target organs during the first 48 h of infection. By 72 to 96 h postinfection, however, numbers of Delta chiA bacteria diminished, indicative of an effective immune response to contain infection. The Delta chiA-associated virulence defect could be complemented in trans by wild-type L. monocytogenes, suggesting that secreted ChiA altered a target that resulted in a more permissive host environment for bacterial replication. ChiA secretion resulted in a dramatic decrease in inducible nitric oxide synthase (iNOS) expression, and Delta chiA mutant virulence was restored in NOS2(-/-) mice lacking iNOS. This work is the first to demonstrate modulation of a specific host innate immune response by a bacterial chitinase.en_US
dc.description.sponsorshipThis work was supported by Public Health Service grants AI076693 (to N.P.C. and N.E.F.) and AI083241 (to N.E.F.) from NIAID.en_US
dc.language.isoen_USen_US
dc.publisherAmerican Society for Microbiologyen_US
dc.titleThe Listeria monocytogenes ChiA Chitinase Enhances Virulence through Suppression of Host Innate Immunityen_US
dc.typeArticleen_US


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