{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T13:28:54Z","timestamp":1791206934023,"version":"4.1.0"},"reference-count":38,"publisher":"American Society for Microbiology","issue":"9","license":[{"start":{"date-parts":[[2013,9,1]],"date-time":"2013-09-01T00:00:00Z","timestamp":1377993600000},"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":[[2013,9]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            Na\n            <jats:sup>+<\/jats:sup>\n            \/H\n            <jats:sup>+<\/jats:sup>\n            antiporters are ubiquitous membrane proteins that play a central role in the ion homeostasis of cells. In this study, we examined the possible role of Na\n            <jats:sup>+<\/jats:sup>\n            \/H\n            <jats:sup>+<\/jats:sup>\n            antiport in\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">Yersinia pestis<\/jats:named-content>\n            virulence and found that\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">Y. pestis<\/jats:named-content>\n            strains lacking the major Na\n            <jats:sup>+<\/jats:sup>\n            \/H\n            <jats:sup>+<\/jats:sup>\n            antiporters, NhaA and NhaB, are completely attenuated in an\n            <jats:italic>in vivo<\/jats:italic>\n            model of plague. The\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">Y. pestis<\/jats:named-content>\n            derivative strain lacking the\n            <jats:italic>nhaA<\/jats:italic>\n            and\n            <jats:italic>nhaB<\/jats:italic>\n            genes showed markedly decreased survival in blood and blood serum\n            <jats:italic>ex vivo<\/jats:italic>\n            . Complementation of either\n            <jats:italic>nhaA<\/jats:italic>\n            or\n            <jats:italic>nhaB<\/jats:italic>\n            in\n            <jats:italic>trans<\/jats:italic>\n            restored the survival of the\n            <jats:italic>Y. pestis nhaA nhaB<\/jats:italic>\n            double deletion mutant in blood. The\n            <jats:italic>nhaA nhaB<\/jats:italic>\n            double deletion mutant also showed inhibited growth in an artificial serum medium, Opti-MEM, and a rich LB-based medium with Na\n            <jats:sup>+<\/jats:sup>\n            levels and pH values similar to those for blood. Taken together, these data strongly suggest that intact Na\n            <jats:sup>+<\/jats:sup>\n            \/H\n            <jats:sup>+<\/jats:sup>\n            antiport is indispensable for the survival of\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">Y. pestis<\/jats:named-content>\n            in the bloodstreams of infected animals and thus might be regarded as a promising noncanonical drug target for infections caused by\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">Y. pestis<\/jats:named-content>\n            and possibly for those caused by other blood-borne bacterial pathogens.\n          <\/jats:p>","DOI":"10.1128\/iai.00071-13","type":"journal-article","created":{"date-parts":[[2013,6,18]],"date-time":"2013-06-18T03:05:15Z","timestamp":1371524715000},"page":"3163-3172","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":51,"title":["Na\n            <sup>+<\/sup>\n            \/H\n            <sup>+<\/sup>\n            Antiport Is Essential for Yersinia pestis Virulence"],"prefix":"10.1128","volume":"81","author":[{"given":"Yusuke","family":"Minato","sequence":"first","affiliation":[{"name":"Department of Biomedical Sciences, College of Veterinary Medicine, Oregon State University, Corvallis, Oregon, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Amit","family":"Ghosh","sequence":"additional","affiliation":[{"name":"Department of Biomedical Sciences, College of Veterinary Medicine, Oregon State University, Corvallis, Oregon, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wyatt J.","family":"Faulkner","sequence":"additional","affiliation":[{"name":"Department of Microbiology, College of Science, Oregon State University, Corvallis, Oregon, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Erin J.","family":"Lind","sequence":"additional","affiliation":[{"name":"Department of Biomedical Sciences, College of Veterinary Medicine, Oregon State University, Corvallis, Oregon, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sara","family":"Schesser Bartra","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, University of Miami, Miller School of Medicine, Miami, Florida, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gregory V.","family":"Plano","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, University of Miami, Miller School of Medicine, Miami, Florida, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Clayton O.","family":"Jarrett","sequence":"additional","affiliation":[{"name":"Laboratory of Zoonotic Pathogens, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"B. 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