Show simple item record

dc.contributor.authorHuston, Wilhelmina M
dc.contributor.authorBarker, Christopher J
dc.contributor.authorChacko, Anu
dc.contributor.authorTimms, Peter
dc.date.accessioned2019-10-30T06:56:44Z
dc.date.available2019-10-30T06:56:44Z
dc.date.issued2014
dc.identifier.issn0021-9193
dc.identifier.doi10.1128/jb.01476-14
dc.identifier.urihttp://hdl.handle.net/10072/388790
dc.description.abstractThe chlamydiae are obligate intracellular parasites that have evolved specific interactions with their various hosts and host cell types to ensure their successful survival and consequential pathogenesis. The species Chlamydia pneumoniae is ubiquitous, with serological studies showing that most humans are infected at some stage in their lifetime. While most human infections are asymptomatic, C. pneumoniae can cause more-severe respiratory disease and pneumonia and has been linked to chronic diseases such as asthma, atherosclerosis, and even Alzheimer's disease. The widely dispersed animal-adapted C. pneumoniae strains cause an equally wide range of diseases in their hosts. It is emerging that the ability of C. pneumoniae to survive inside its target cells, including evasion of the host's immune attack mechanisms, is linked to the acquisition of key metabolites. Tryptophan and arginine are key checkpoint compounds in this host-parasite battle. Interestingly, the animal strains of C. pneumoniae have a slightly larger genome, enabling them to cope better with metabolite restrictions. It therefore appears that as the evolutionarily more ancient animal strains have evolved to infect humans, they have selectively become more “susceptible” to the levels of key metabolites, such as tryptophan. While this might initially appear to be a weakness, it allows these human C. pneumoniae strains to exquisitely sense host immune attack and respond by rapidly reverting to a persistent phase. During persistence, they reduce their metabolic levels, halting progression of their developmental cycle, waiting until the hostile external conditions have passed before they reemerge.
dc.description.peerreviewedYes
dc.languageEnglish
dc.language.isoeng
dc.publisherAmerican Society for Microbiology
dc.relation.ispartofpagefrom1915
dc.relation.ispartofpageto1924
dc.relation.ispartofissue11
dc.relation.ispartofjournalJournal of Bacteriology
dc.relation.ispartofvolume196
dc.subject.fieldofresearchBiological Sciences
dc.subject.fieldofresearchAgricultural and Veterinary Sciences
dc.subject.fieldofresearchMedical and Health Sciences
dc.subject.fieldofresearchcode06
dc.subject.fieldofresearchcode07
dc.subject.fieldofresearchcode11
dc.titleEvolution to a Chronic Disease Niche Correlates with Increased Sensitivity to Tryptophan Availability for the Obligate Intracellular Bacterium Chlamydia pneumoniae
dc.typeJournal article
dc.type.descriptionC1 - Articles
dcterms.bibliographicCitationHuston, WM; Barker, CJ; Chacko, A; Timms, P, Evolution to a Chronic Disease Niche Correlates with Increased Sensitivity to Tryptophan Availability for the Obligate Intracellular Bacterium Chlamydia pneumoniae, Journal of Bacteriology, 2014, 196 (11), pp. 1915-1924
dc.date.updated2019-10-29T02:09:29Z
dc.description.versionVersion of Record (VoR)
gro.rights.copyright© 2015 American Society for Microbiology. The attached file is reproduced here in accordance with the copyright policy of the publisher. Please refer to the journal's website for access to the definitive, published version.
gro.hasfulltextFull Text
gro.griffith.authorChacko, Anu


Files in this item

This item appears in the following Collection(s)

  • Journal articles
    Contains articles published by Griffith authors in scholarly journals.

Show simple item record