{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,30]],"date-time":"2026-10-30T11:56:55Z","timestamp":1793361415832,"version":"4.5.0"},"reference-count":48,"publisher":"American Society for Microbiology","issue":"3","license":[{"start":{"date-parts":[[2014,3,1]],"date-time":"2014-03-01T00:00:00Z","timestamp":1393632000000},"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":[[2014,3]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            <jats:named-content content-type=\"genus-species\">Klebsiella pneumoniae<\/jats:named-content>\n            liver abscess (KPLA) is prevalent in East Asia. Liver abscess can develop after translocation of\n            <jats:named-content content-type=\"genus-species\">K. pneumoniae<\/jats:named-content>\n            from a patient's bowel into the liver via the portal circulation. TREM-1 (\n            <jats:italic>t<\/jats:italic>\n            riggering\n            <jats:italic>r<\/jats:italic>\n            eceptor\n            <jats:italic>e<\/jats:italic>\n            xpressed on\n            <jats:italic>m<\/jats:italic>\n            yeloid cells\n            <jats:italic>1<\/jats:italic>\n            ) amplifies inflammatory signaling during infection, but its role in KPLA is poorly understood. We used an animal study to characterize the role of TREM-1 in KPLA. We compared survival rates, bacterial burdens in tissues, inflammatory cytokine levels, and histology findings between wild-type and\n            <jats:italic>Trem-1<\/jats:italic>\n            knockout (KO) mice after oral inoculation of capsular type K1\n            <jats:named-content content-type=\"genus-species\">K. pneumoniae<\/jats:named-content>\n            . Translocation of\n            <jats:named-content content-type=\"genus-species\">K. pneumoniae<\/jats:named-content>\n            to mesenteric lymph nodes and liver was examined, and intestinal permeability, antimicrobial peptide expression, and the clearance of\n            <jats:named-content content-type=\"genus-species\">K. pneumoniae<\/jats:named-content>\n            in the small intestine were determined. In the absence of TREM-1, KPLA model mice showed increased\n            <jats:named-content content-type=\"genus-species\">K. pneumoniae<\/jats:named-content>\n            dissemination, enhanced liver and systemic inflammation, and reduced survival. Impaired bacterial clearance in the small intestine causes enhanced\n            <jats:named-content content-type=\"genus-species\">K. pneumoniae<\/jats:named-content>\n            translocation, which renders\n            <jats:italic>Trem-1<\/jats:italic>\n            KO mice more susceptible to\n            <jats:named-content content-type=\"genus-species\">K. pneumoniae<\/jats:named-content>\n            oral infection. In conclusion, TREM-1-mediated bacterial clearance in the small intestine is an important immune response against\n            <jats:named-content content-type=\"genus-species\">K. pneumoniae<\/jats:named-content>\n            . TREM-1 deficiency enhances\n            <jats:named-content content-type=\"genus-species\">K. pneumoniae<\/jats:named-content>\n            translocation in the small intestine and increases mortality rates in mice with KPLA.\n          <\/jats:p>","DOI":"10.1128\/iai.01347-13","type":"journal-article","created":{"date-parts":[[2014,1,7]],"date-time":"2014-01-07T04:37:56Z","timestamp":1389069476000},"page":"1335-1342","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":37,"title":["TREM-1 Promotes Survival during Klebsiella pneumoniae Liver Abscess in Mice"],"prefix":"10.1128","volume":"82","author":[{"given":"Yi-Tsung","family":"Lin","sequence":"first","affiliation":[{"name":"Division of Infectious Diseases, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan"},{"name":"Institute of Clinical Medicine, National Yang-Ming University, Taipei, Taiwan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kai-Yu","family":"Tseng","sequence":"additional","affiliation":[{"name":"Institute of Microbiology and Immunology, National Yang-Ming University, Taipei, Taiwan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yi-Chen","family":"Yeh","sequence":"additional","affiliation":[{"name":"Department of Pathology and Laboratory Medicine, Taipei Veterans General Hospital, Taipei, Taiwan"},{"name":"Department of Medicine, School of Medicine, National Yang-Ming University, Taipei, Taiwan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fu-Chen","family":"Yang","sequence":"additional","affiliation":[{"name":"Institute of Microbiology and Immunology, National Yang-Ming University, Taipei, Taiwan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chang-Phone","family":"Fung","sequence":"additional","affiliation":[{"name":"Division of Infectious Diseases, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan"},{"name":"Institute of Emergency and Critical Care Medicine, National Yang-Ming University, Taipei, Taiwan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nien-Jung","family":"Chen","sequence":"additional","affiliation":[{"name":"Institute of Microbiology and Immunology, National Yang-Ming University, Taipei, Taiwan"},{"name":"Infection and Immunity Research Center, National Yang-Ming University, Taipei, 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