{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T17:11:56Z","timestamp":1791047516221,"version":"4.1.0"},"reference-count":32,"publisher":"American Society for Microbiology","issue":"2","license":[{"start":{"date-parts":[[2014,2,1]],"date-time":"2014-02-01T00:00:00Z","timestamp":1391212800000},"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":[[2014,2]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            Pathogen transmission cycles require many steps: initial colonization, growth and persistence, shedding, and transmission to new hosts. Alterations in the membrane components of the bacteria, including lipid A, the membrane anchor of lipopolysaccharide, could affect any of these steps via its structural role protecting bacteria from host innate immune defenses, including antimicrobial peptides and signaling through Toll-like receptor 4 (TLR4). To date, lipid A has been shown to affect only the within-host dynamics of infection, not the between-host dynamics of transmission. Here, we investigate the effects of lipid A modification in a mouse infection and transmission model. Disruption of the\n            <jats:named-content content-type=\"genus-species\">Bordetella bronchiseptica<\/jats:named-content>\n            locus (\n            <jats:italic>BB4268<\/jats:italic>\n            ) revealed that ArnT is required for addition of glucosamine (GlcN) to\n            <jats:named-content content-type=\"genus-species\">B. bronchiseptica<\/jats:named-content>\n            lipid A. ArnT modification of lipid A did not change its TLR4 agonist activity in J774 cells, but deleting\n            <jats:italic>arnT<\/jats:italic>\n            decreased resistance to killing by cationic antimicrobial peptides, such as polymyxin B and \u03b2-defensins. In the standard infection model, mutation of\n            <jats:italic>arnT<\/jats:italic>\n            did not affect\n            <jats:named-content content-type=\"genus-species\">B. bronchiseptica<\/jats:named-content>\n            colonization, growth, persistence throughout the respiratory tract, recruitment of neutrophils to the nasal cavity, or shedding of the pathogen. However, the number of bacteria necessary to colonize a host (50% infective dose [ID\n            <jats:sub>50<\/jats:sub>\n            ]) was 5-fold higher for the\n            <jats:italic>arnT<\/jats:italic>\n            mutant. Furthermore, the\n            <jats:italic>arnT<\/jats:italic>\n            mutant was defective in transmission between hosts. These results reveal novel functions of the ArnT lipid A modification and highlight the sensitivity of low-dose infections and transmission experiments for illuminating aspects of infectious diseases between hosts. Factors such as ArnT can have important effects on the burden of disease and are potential targets for interventions that can interrupt transmission.\n          <\/jats:p>","DOI":"10.1128\/iai.01260-12","type":"journal-article","created":{"date-parts":[[2013,10,15]],"date-time":"2013-10-15T00:16:11Z","timestamp":1381796171000},"page":"491-499","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":23,"title":["Enzymatic Modification of Lipid A by ArnT Protects Bordetella bronchiseptica against Cationic Peptides and Is Required for Transmission"],"prefix":"10.1128","volume":"82","author":[{"given":"Olivier","family":"Rolin","sequence":"first","affiliation":[{"name":"Department of Veterinary and Biomedical Sciences, The Pennsylvania State University, University Park, Pennsylvania, USA"},{"name":"Graduate Program in Immunology and Infectious Disease, The Pennsylvania State University, University Park, Pennsylvania, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sarah J.","family":"Muse","sequence":"additional","affiliation":[{"name":"Department of Veterinary and Biomedical Sciences, The Pennsylvania State University, University Park, Pennsylvania, USA"},{"name":"Graduate Program in Biochemistry, Microbiology and Molecular Biology, The Pennsylvania State University, University Park, Pennsylvania, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chetan","family":"Safi","sequence":"additional","affiliation":[{"name":"Department of Veterinary and Biomedical Sciences, The Pennsylvania State University, University Park, Pennsylvania, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shokrollah","family":"Elahi","sequence":"additional","affiliation":[{"name":"Seattle Biomedical Research Institute, Seattle, Washington, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Volker","family":"Gerdts","sequence":"additional","affiliation":[{"name":"Vaccine and Infectious Disease Organization, University of Saskatchewan, Saskatoon, Saskatchewan, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lauren E.","family":"Hittle","sequence":"additional","affiliation":[{"name":"Department of Microbial Pathogenesis, University of Maryland School of Dentistry, Baltimore, Maryland, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Robert K.","family":"Ernst","sequence":"additional","affiliation":[{"name":"Department of Microbial Pathogenesis, University of Maryland School of Dentistry, Baltimore, Maryland, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eric T.","family":"Harvill","sequence":"additional","affiliation":[{"name":"Department of Veterinary and Biomedical Sciences, The Pennsylvania State University, University Park, 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