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We tested the hypothesis that human strains of <jats:styled-content style=\"fixed-case\"><jats:italic>C<\/jats:italic><\/jats:styled-content><jats:italic>hlamydia pneumoniae<\/jats:italic> are more sensitive to tryptophan limitation than animal <jats:styled-content style=\"fixed-case\"><jats:italic>C<\/jats:italic><\/jats:styled-content><jats:italic>. pneumoniae<\/jats:italic> strains. The human strains were significantly more sensitive to <jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content>\u2010\u03b3 than the animal strains in a lung epithelia cell model (<jats:styled-content style=\"fixed-case\">BEAS<\/jats:styled-content>\u20102<jats:styled-content style=\"fixed-case\">B<\/jats:styled-content>), with exposure to 1\u2009U\u2009ml<jats:sup>\u22121<\/jats:sup> <jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content>\u2010\u03b3 resulting in complete loss of infectious yield of human strains, compared to the animal strains where reductions in infectious progeny were around 3.5\u20134.0 log. Strikingly, the <jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content>\u2010\u03b3 induced loss of ability to form infectious progeny production was completely rescued by removal of the <jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content>\u2010\u03b3 and addition of exogenous tryptophan for the human strains, but not the animal strains. In fact, a human heart strain was more capable of entering a non\u2010infectious, viable persistent stage when exposed to <jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content>\u2010\u03b3 and was also more effectively rescued, compared to a human respiratory strain. Exquisite susceptibility to <jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content>\u2010\u03b3, specifically due to tryptophan availability appears to be a core adaptation of the human <jats:styled-content style=\"fixed-case\"><jats:italic>C<\/jats:italic><\/jats:styled-content><jats:italic>. pneumoniae<\/jats:italic> strains, which may reflect the chronic nature of their infections in this host.<\/jats:p>","DOI":"10.1111\/mmi.12701","type":"journal-article","created":{"date-parts":[[2014,7,3]],"date-time":"2014-07-03T06:23:15Z","timestamp":1404368595000},"page":"797-813","source":"Crossref","is-referenced-by-count":16,"title":["Increased sensitivity to tryptophan bioavailability is a positive adaptation by the human strains of <scp><i>C<\/i><\/scp><i>hlamydia pneumoniae<\/i>"],"prefix":"10.1111","volume":"93","author":[{"given":"Anu","family":"Chacko","sequence":"first","affiliation":[{"name":"Institute of Health and Biomedical Innovation School of Biomedical Sciences Faculty of Health Queensland University of Technology  60 Musk Ave Kelvin Grove Qld 4059 Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christopher J.","family":"Barker","sequence":"additional","affiliation":[{"name":"Institute of Health and Biomedical Innovation School of Biomedical Sciences Faculty of Health Queensland University of Technology  60 Musk Ave Kelvin Grove Qld 4059 Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kenneth W.","family":"Beagley","sequence":"additional","affiliation":[{"name":"Institute of Health and Biomedical Innovation School of Biomedical Sciences Faculty of Health Queensland University of Technology  60 Musk Ave Kelvin Grove Qld 4059 Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mark P.","family":"Hodson","sequence":"additional","affiliation":[{"name":"Metabolomics Australia (Queensland Node) Australian Institute for Bioengineering and Nanotechnology The University of 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