{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T12:15:17Z","timestamp":1791288917788,"version":"4.3.0"},"reference-count":45,"publisher":"American Society for Microbiology","issue":"3","license":[{"start":{"date-parts":[[2010,3,1]],"date-time":"2010-03-01T00:00:00Z","timestamp":1267401600000},"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":[[2010,3]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:p><jats:italic>Pseudomonas aeruginosa<\/jats:italic>, a major respiratory pathogen in cystic fibrosis (CF) patients, facilitates infection by other opportunistic pathogens.<jats:italic>Burkholderia cenocepacia<\/jats:italic>, which normally infects adolescent patients, encounters alginate elaborated by mucoid<jats:italic>P. aeruginosa<\/jats:italic>. To determine whether<jats:italic>P. aeruginosa<\/jats:italic>alginate facilitates<jats:italic>B. cenocepacia<\/jats:italic>infection in mice, cystic fibrosis transmembrane conductance regulator knockout mice were infected with<jats:italic>B. cenocepacia<\/jats:italic>strain BC7 suspended in either phosphate-buffered saline (BC7\/PBS) or<jats:italic>P. aeruginosa<\/jats:italic>alginate (BC7\/alginate), and the pulmonary bacterial load and inflammation were monitored. Mice infected with BC7\/PBS cleared all of the bacteria within 3 days, and inflammation was resolved by day 5. In contrast, mice infected with BC7\/alginate showed persistence of bacteria and increased cytokine levels for up to 7 days. Histological examination of the lungs indicated that there was moderate to severe inflammation and pneumonic consolidation in isolated areas at 5 and 7 days postinfection in the BC7\/alginate group. Further, alginate decreased phagocytosis of<jats:italic>B. cenocepacia<\/jats:italic>by professional phagocytes both<jats:italic>in vivo<\/jats:italic>and<jats:italic>in vitro. P. aeruginosa<\/jats:italic>alginate also reduced the proinflammatory responses of CF airway epithelial cells and alveolar macrophages to<jats:italic>B. cenocepacia<\/jats:italic>infection. The observed effects are specific to<jats:italic>P. aeruginosa<\/jats:italic>alginate, because enzymatically degraded alginate or other polyuronic acids did not facilitate bacterial persistence. These observations suggest that<jats:italic>P. aeruginosa<\/jats:italic>alginate may facilitate<jats:italic>B. cenocepacia<\/jats:italic>infection by interfering with host innate defense mechanisms.<\/jats:p>","DOI":"10.1128\/iai.01192-09","type":"journal-article","created":{"date-parts":[[2010,1,5]],"date-time":"2010-01-05T02:10:40Z","timestamp":1262657440000},"page":"984-993","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":32,"title":["<i>Pseudomonas aeruginosa<\/i>Alginate Promotes<i>Burkholderia cenocepacia<\/i>Persistence in Cystic Fibrosis Transmembrane Conductance Regulator Knockout Mice"],"prefix":"10.1128","volume":"78","author":[{"given":"Sangbrita S.","family":"Chattoraj","sequence":"first","affiliation":[{"name":"Department of Pediatrics and Communicable Diseases"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rachana","family":"Murthy","sequence":"additional","affiliation":[{"name":"Department of Pediatrics and Communicable Diseases"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shyamala","family":"Ganesan","sequence":"additional","affiliation":[{"name":"Department of Pediatrics and Communicable Diseases"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joanna B.","family":"Goldberg","sequence":"additional","affiliation":[{"name":"Department of Microbiology, University of Virginia Health System, Charlottesville, Virginia 22908"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ying","family":"Zhao","sequence":"additional","affiliation":[{"name":"Department of Pediatrics and Communicable Diseases"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marc B.","family":"Hershenson","sequence":"additional","affiliation":[{"name":"Department of Pediatrics and Communicable Diseases"},{"name":"Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, Michigan 48109"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Umadevi S.","family":"Sajjan","sequence":"additional","affiliation":[{"name":"Department of Pediatrics and Communicable Diseases"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1203\/00006450-198710000-00013"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0144-8617(03)00144-9"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.70.3.1081-1086.2002"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1128\/CMR.4.1.35"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1128\/mr.60.3.539-574.1996"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1038\/nature07811"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1099\/mic.0.2006\/004077-0"},{"key":"e_1_3_2_9_2","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119828"},{"key":"e_1_3_2_10_2","doi-asserted-by":"publisher","DOI":"10.1128\/jcm.35.3.614-619.1997"},{"key":"e_1_3_2_11_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-3476(84)80993-2"},{"key":"e_1_3_2_12_2","first-page":"279","volume":"55","year":"2005","unstructured":"Kashef, N., Q. 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