{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,19]],"date-time":"2026-09-19T09:29:48Z","timestamp":1789810188391,"version":"4.0.1"},"reference-count":53,"publisher":"American Society for Microbiology","issue":"9","license":[{"start":{"date-parts":[[2008,9,1]],"date-time":"2008-09-01T00:00:00Z","timestamp":1220227200000},"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":["Antimicrob Agents Chemother"],"published-print":{"date-parts":[[2008,9]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            Extended-spectrum \u03b2-lactamase (ESBL)-producing\n            <jats:italic>Klebsiella pneumoniae<\/jats:italic>\n            strains are suggested to possess higher pathogenic potential than non-ESBL producers. Microbial adherence to and invasion of host cells are critical steps in the infection process, so we examined the expression of type 1 and 3 fimbrial adhesins by 58 ESBL-producing and 152 nonproducing isolates of\n            <jats:italic>K. pneumoniae<\/jats:italic>\n            and their abilities to invade ileocecal and bladder epithelial cells. Mannose-sensitive hemagglutination of guinea pig erythrocytes and mannose-resistant hemagglutination of ox erythrocytes were evaluated to determine the strains\u2019 abilities to express type 1 and type 3 fimbriae, respectively. Bacterial adhesion to and invasion of epithelial cells were tested by enzyme-linked immunosorbent assay and imipenem killing assay, respectively. The adherence of ESBL- and non-ESBL-producing strains to epithelial cells did not differ significantly (\n            <jats:italic>P<\/jats:italic>\n            &gt; 0.05). In contrast, the proportion of strains capable of invading (&gt;5% relative invasion) ileocecal and bladder epithelial cells was significantly higher among ESBL producers (81%,\n            <jats:italic>n<\/jats:italic>\n            = 47\/58, and 27.6%,\n            <jats:italic>n<\/jats:italic>\n            = 16\/58, respectively) than among non-ESBL producers (61%,\n            <jats:italic>n<\/jats:italic>\n            = 93\/152, and 10%,\n            <jats:italic>n<\/jats:italic>\n            = 15\/152, respectively) (\n            <jats:italic>P<\/jats:italic>\n            = 0.0084, odds ratio [OR] = 2.711, 95% confidence interval [CI] = 1.302 to 5.643 and\n            <jats:italic>P<\/jats:italic>\n            = 0.0021, OR = 4.79, 95% CI = 1.587 to 7.627). The mean invasion by ESBL producers (5.5% \u00b1 2.8% and 3.3% \u00b1 2.7%, respectively) was significantly higher than that by non-ESBL producers (2.9% \u00b1 2.6% and 1.8% \u00b1 2%, respectively) (\n            <jats:italic>P<\/jats:italic>\n            &lt; 0.0001). Likewise, the proportion of ESBL producers coexpressing both fimbrial adhesins was significantly higher (79.3%;\n            <jats:italic>n<\/jats:italic>\n            = 46\/58) than that of non-ESBL producers (61.8%;\n            <jats:italic>n<\/jats:italic>\n            = 94\/152) (\n            <jats:italic>P<\/jats:italic>\n            = 0.0214; OR = 2,365; 95% CI = 1.157 to 4.834). Upon acquisition of SHV-12-encoding plasmids, two transconjugants switched on to produce type 3 fimbriae while expression of type 1 fimbriae was not affected. The acquisition of an ESBL plasmid appeared to upregulate the phenotypic expression of one or more genes, resulting in greater invasion ability.\n          <\/jats:p>","DOI":"10.1128\/aac.00010-08","type":"journal-article","created":{"date-parts":[[2008,6,24]],"date-time":"2008-06-24T01:07:28Z","timestamp":1214269648000},"page":"3029-3034","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":82,"title":["Extended-Spectrum \u03b2-Lactamase Production Is Associated with an Increase in Cell Invasion and Expression of Fimbrial Adhesins in\n            <i>Klebsiella pneumoniae<\/i>"],"prefix":"10.1128","volume":"52","author":[{"given":"H.","family":"Sahly","sequence":"first","affiliation":[{"name":"Institute for Infection Medicine, Faculty of Medicine, University of Kiel, Kiel"},{"name":"IPM-Biotech Institute for Immunology, Clinical Pathology and Molecular Medicine, Hamburg, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S.","family":"Navon-Venezia","sequence":"additional","affiliation":[{"name":"Division of Epidemiology, Tel Aviv Sourasky Medical Center, Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"L.","family":"Roesler","sequence":"additional","affiliation":[{"name":"Department of Anaesthesiology and Intensive Care Medicine, University Hospital Schleswig-Holstein, Campus Kiel, Kiel, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A.","family":"Hay","sequence":"additional","affiliation":[{"name":"Division of Epidemiology, Tel Aviv Sourasky Medical Center, Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Y.","family":"Carmeli","sequence":"additional","affiliation":[{"name":"Division of Epidemiology, Tel Aviv Sourasky Medical Center, Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"R.","family":"Podschun","sequence":"additional","affiliation":[{"name":"Institute for Infection Medicine, Faculty of Medicine, University of Kiel, Kiel"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"C.","family":"Hennequin","sequence":"additional","affiliation":[{"name":"Laboratoire de Bacte\u0301riologie, Faculte\u0301 de Pharmacie, Universite\u0301 de Clermont 1, Clermont-Ferrand, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"C.","family":"Forestier","sequence":"additional","affiliation":[{"name":"Laboratoire de Bacte\u0301riologie, Faculte\u0301 de Pharmacie, Universite\u0301 de Clermont 1, Clermont-Ferrand, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"I.","family":"Ofek","sequence":"additional","affiliation":[{"name":"Department of Human Microbiology, University of Tel Aviv, Tel Aviv, Israel"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_1_2_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.93.18.9827"},{"key":"e_1_3_1_3_2","doi-asserted-by":"publisher","DOI":"10.1128\/iai.60.1.44-55.1992"},{"key":"e_1_3_1_4_2","doi-asserted-by":"publisher","DOI":"10.1128\/iai.64.8.2998-3006.1996"},{"key":"e_1_3_1_5_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0923-2508(02)00004-9"},{"key":"e_1_3_1_6_2","doi-asserted-by":"publisher","DOI":"10.1128\/jcm.35.6.1499-1503.1997"},{"key":"e_1_3_1_7_2","doi-asserted-by":"publisher","DOI":"10.1128\/iai.64.6.2266-2273.1996"},{"key":"e_1_3_1_8_2","doi-asserted-by":"crossref","first-page":"451","DOI":"10.1086\/515159","volume":"28","year":"1999","unstructured":"Donnenberg, M. 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