{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,12]],"date-time":"2026-03-12T02:38:19Z","timestamp":1773283099914,"version":"3.50.1"},"reference-count":20,"publisher":"American Society for Microbiology","issue":"2","license":[{"start":{"date-parts":[[2011,2,1]],"date-time":"2011-02-01T00:00:00Z","timestamp":1296518400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Infect Immun"],"published-print":{"date-parts":[[2011,2]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            The interaction between\n            <jats:italic>Salmonella enterica<\/jats:italic>\n            and the host immune system is complex. The outcome of an infection is the result of a balance between the\n            <jats:italic>in vivo<\/jats:italic>\n            environment where the bacteria survive and grow and the regulation of fitness genes at a level sufficient for the bacteria to retain their characteristic rate of growth in a given host. Using bacteriological counts from tissue homogenates and fluorescence microscopy to determine the spread, localization, and distribution of\n            <jats:italic>S. enterica<\/jats:italic>\n            in the tissues, we show that, during a systemic infection,\n            <jats:italic>S. enterica<\/jats:italic>\n            adapts to the\n            <jats:italic>in vivo<\/jats:italic>\n            environment. The adaptation becomes a measurable phenotype when bacteria that have resided in a donor animal are introduced into a recipient nai\u0308ve animal. This adaptation does not confer increased resistance to early host killing mechanisms but can be detected as an enhancement in the bacterial net growth rate later in the infection. The enhanced growth rate is lost upon a single passage\n            <jats:italic>in vitro<\/jats:italic>\n            , and it is therefore transient and not due to selection of mutants. The adapted bacteria on average reach higher intracellular numbers in individual infected cells and therefore have patterns of organ spread different from those of nonadapted bacteria. These experiments help in developing an understanding of the influence of passage in a host on the fitness and virulence of\n            <jats:italic>S. enterica<\/jats:italic>\n            .\n          <\/jats:p>","DOI":"10.1128\/iai.00954-10","type":"journal-article","created":{"date-parts":[[2010,11,23]],"date-time":"2010-11-23T04:07:46Z","timestamp":1290485266000},"page":"636-643","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":27,"title":["Enhanced Virulence of\n            <i>Salmonella enterica<\/i>\n            Serovar Typhimurium after Passage through Mice"],"prefix":"10.1128","volume":"79","author":[{"given":"Pietro","family":"Mastroeni","sequence":"first","affiliation":[{"name":"Department of Veterinary Medicine, University of Cambridge, Madingley Road, Cambridge CB3 0ES, United Kingdom"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Fiona J. E.","family":"Morgan","sequence":"additional","affiliation":[{"name":"Department of Veterinary Medicine, University of Cambridge, Madingley Road, Cambridge CB3 0ES, United Kingdom"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Trevelyan J.","family":"McKinley","sequence":"additional","affiliation":[{"name":"Cambridge Infectious Diseases Consortium, Department of Veterinary Medicine, University of Cambridge, Madingley Road, Cambridge CB3 0ES, United Kingdom"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ewan","family":"Shawcroft","sequence":"additional","affiliation":[{"name":"Department of Veterinary Medicine, University of Cambridge, Madingley Road, Cambridge CB3 0ES, United Kingdom"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Simon","family":"Clare","sequence":"additional","affiliation":[{"name":"Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge CB10 1SA, United Kingdom"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Duncan J.","family":"Maskell","sequence":"additional","affiliation":[{"name":"Department of Veterinary Medicine, University of Cambridge, Madingley Road, Cambridge CB3 0ES, United Kingdom"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Andrew J.","family":"Grant","sequence":"additional","affiliation":[{"name":"Department of Veterinary Medicine, University of Cambridge, Madingley Road, Cambridge CB3 0ES, United Kingdom"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"235","reference":[{"key":"e_1_3_3_2_2","first-page":"2091","volume":"4","year":"2006","unstructured":"Brown, S. 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