{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T01:31:41Z","timestamp":1787016701246,"version":"build-2736575974"},"reference-count":46,"publisher":"American Society for Microbiology","issue":"3","license":[{"start":{"date-parts":[[2018,3,1]],"date-time":"2018-03-01T00:00:00Z","timestamp":1519862400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"funder":[{"DOI":"10.13039\/100000060","name":"HHS | NIH | National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["AI112258"],"award-info":[{"award-number":["AI112258"]}],"id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000060","name":"HHS | NIH | National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["AI109799"],"award-info":[{"award-number":["AI109799"]}],"id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000060","name":"HHS | NIH | National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["AI118807"],"award-info":[{"award-number":["AI118807"]}],"id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000060","name":"HHS | NIH | National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["AI128151"],"award-info":[{"award-number":["AI128151"]}],"id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Infect Immun"],"published-print":{"date-parts":[[2018,3]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Treatment of intracellular bacterial pathogens with antibiotic therapy often requires a long course of multiple drugs. A barrier to developing strategies that enhance antibiotic efficacy against these pathogens is our poor understanding of the intracellular nutritional environment that maintains bacterial persistence. The intracellular pathogen\n                    <jats:named-content content-type=\"genus-species\">Brucella abortus<\/jats:named-content>\n                    survives and replicates preferentially in alternatively activated macrophages (AAMs); however, knowledge of the metabolic adaptations promoting exploitation of this niche is limited. Here we show that one mechanism promoting enhanced survival in AAMs is a shift in macrophage arginine utilization from production of nitric oxide (NO) to biosynthesis of polyamines, induced by interleukin 4 (IL-4)\/IL-13 treatment. Production of polyamines by infected AAMs promoted both intracellular survival of\n                    <jats:named-content content-type=\"genus-species\">B. abortus<\/jats:named-content>\n                    and chronic infection in mice, as inhibition of macrophage polyamine synthesis or inactivation of the putative putrescine transporter encoded by\n                    <jats:italic>potIHGF<\/jats:italic>\n                    reduced both intracellular survival in AAMs and persistence in mice. These results demonstrate that increased intracellular availability of polyamines induced by arginase-1 expression in IL-4\/IL-13-induced AAMs promotes chronic persistence of\n                    <jats:named-content content-type=\"genus-species\">B. abortus<\/jats:named-content>\n                    within this niche and suggest that targeting of this pathway may aid in eradicating chronic infection.\n                  <\/jats:p>","DOI":"10.1128\/iai.00458-17","type":"journal-article","created":{"date-parts":[[2017,12,4]],"date-time":"2017-12-04T11:36:43Z","timestamp":1512387403000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":22,"title":["Utilization of Host Polyamines in Alternatively Activated Macrophages Promotes Chronic Infection by Brucella abortus"],"prefix":"10.1128","volume":"86","author":[{"given":"Tobias","family":"Kerrinnes","sequence":"first","affiliation":[{"name":"Department of Medical Microbiology 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