{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,23]],"date-time":"2026-10-23T05:46:55Z","timestamp":1792734415729,"version":"4.5.0"},"reference-count":31,"publisher":"American Society for Microbiology","issue":"5","license":[{"start":{"date-parts":[[2004,5,1]],"date-time":"2004-05-01T00:00:00Z","timestamp":1083369600000},"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":[[2004,5]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            <jats:italic>Escherichia coli<\/jats:italic>\n            is a common cause of meningitis and sepsis in the newborn infant, and the large majority of isolates from these infections produce a polysialic acid (PSA) capsular polysaccharide, the K1 antigen, that protects the bacterial cell from immune attack. We determined whether a capsule-depolymerizing enzyme, by removing this protective barrier, could alter the outcome of systemic infection in an animal model. Bacteriophage-derived endosialidase E (endoE) selectively degrades the PSA capsule on the surface of\n            <jats:italic>E. coli<\/jats:italic>\n            K1 strains. Intraperitoneal administration of small quantities of recombinant endoE (20 \u03bcg) to 3-day-old rats, colonized with a virulent strain of K1, prevented bacteremia and death from systemic infection. The enzyme had no effect on the viability of\n            <jats:italic>E. coli<\/jats:italic>\n            strains but sensitized strains expressing PSA to killing by the complement system. This study demonstrates the potential therapeutic efficacy of agents that cure infections by modification of the bacterial phenotype rather than by killing or inhibition of growth of the pathogen.\n          <\/jats:p>","DOI":"10.1128\/aac.48.5.1503-1508.2004","type":"journal-article","created":{"date-parts":[[2004,4,22]],"date-time":"2004-04-22T19:58:16Z","timestamp":1082663896000},"page":"1503-1508","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":98,"title":["Prevention and Cure of Systemic\n            <i>Escherichia coli<\/i>\n            K1 Infection by Modification of the Bacterial Phenotype"],"prefix":"10.1128","volume":"48","author":[{"given":"Naseem","family":"Mushtaq","sequence":"first","affiliation":[{"name":"Microbiology Group, School of Pharmacy, London WC1N 1AX"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maria B.","family":"Redpath","sequence":"additional","affiliation":[{"name":"Microbiology Group, School of Pharmacy, London WC1N 1AX"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J. Paul","family":"Luzio","sequence":"additional","affiliation":[{"name":"Cambridge Institute for Medical Research and Department of Clinical Biochemistry, University of Cambridge, Cambridge CB2 2XY, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Peter W.","family":"Taylor","sequence":"additional","affiliation":[{"name":"Microbiology Group, School of Pharmacy, London WC1N 1AX"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1128\/iai.39.1.315-335.1983"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.54.1.73"},{"key":"e_1_3_2_4_2","first-page":"87","volume":"150","year":"1990","unstructured":"Cross, A. S. 1990. The biologic significance of bacterial encapsulation. Curr. Top. Microbiol. Immunol.150:87-95.","journal-title":"Curr. Top. Microbiol. 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