{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T02:37:10Z","timestamp":1790649430896,"version":"4.1.0"},"reference-count":56,"publisher":"American Society for Microbiology","issue":"4","license":[{"start":{"date-parts":[[2015,4,1]],"date-time":"2015-04-01T00:00:00Z","timestamp":1427846400000},"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":[[2015,4]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            <jats:named-content content-type=\"genus-species\">Pseudomonas aeruginosa<\/jats:named-content>\n            is a major bacterial pathogen commonly associated with chronic lung infections in cystic fibrosis (CF). Previously, we have demonstrated that the type IV pilus (Tfp) of\n            <jats:named-content content-type=\"genus-species\">P. aeruginosa<\/jats:named-content>\n            mediates resistance to antibacterial effects of pulmonary surfactant protein A (SP-A). Interestingly,\n            <jats:named-content content-type=\"genus-species\">P. aeruginosa<\/jats:named-content>\n            strains with group I pilins are\n            <jats:italic>O<\/jats:italic>\n            -glycosylated through the TfpO glycosyltransferase with a single subunit of O-antigen (O-ag). Importantly, TfpO-mediated\n            <jats:italic>O<\/jats:italic>\n            -glycosylation is important for virulence in mouse lungs, exemplified by more frequent lung infection in CF with TfpO-expressing\n            <jats:named-content content-type=\"genus-species\">P. aeruginosa<\/jats:named-content>\n            strains. However, the mechanism underlying the importance of Tfp glycosylation in\n            <jats:named-content content-type=\"genus-species\">P. aeruginosa<\/jats:named-content>\n            pathogenesis is not fully understood. Here, we demonstrated one mechanism of increased fitness mediated by\n            <jats:italic>O<\/jats:italic>\n            -glycosylation of group 1 pilins on Tfp in the\n            <jats:named-content content-type=\"genus-species\">P. aeruginosa<\/jats:named-content>\n            clinical isolate 1244. Using an acute pneumonia model in SP-A\n            <jats:sup>+\/+<\/jats:sup>\n            versus SP-A\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            mice, the\n            <jats:italic>O<\/jats:italic>\n            -glycosylation-deficient \u0394\n            <jats:italic>tfpO<\/jats:italic>\n            mutant was found to be attenuated in lung infection. Both 1244 and \u0394\n            <jats:italic>tfpO<\/jats:italic>\n            strains showed equal levels of susceptibility to SP-A-mediated membrane permeability. In contrast, the \u0394\n            <jats:italic>tfpO<\/jats:italic>\n            mutant was more susceptible to opsonization by SP-A and by other pulmonary and circulating opsonins, SP-D and mannose binding lectin 2, respectively. Importantly, the increased susceptibility to phagocytosis was abrogated in the absence of opsonins. These results indicate that\n            <jats:italic>O<\/jats:italic>\n            -glycosylation of Tfp with O-ag specifically confers resistance to opsonization during host-mediated phagocytosis.\n          <\/jats:p>","DOI":"10.1128\/iai.02874-14","type":"journal-article","created":{"date-parts":[[2015,1,21]],"date-time":"2015-01-21T06:01:14Z","timestamp":1421820074000},"page":"1339-1346","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":41,"title":["Type IV Pilus Glycosylation Mediates Resistance of Pseudomonas aeruginosa to Opsonic Activities of the Pulmonary Surfactant Protein A"],"prefix":"10.1128","volume":"83","author":[{"given":"Rommel M.","family":"Tan","sequence":"first","affiliation":[{"name":"Department of Pathobiology, University of Illinois at Urbana-Champaign, Urbana, Illinois, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhizhou","family":"Kuang","sequence":"additional","affiliation":[{"name":"Department of Pathobiology, University of Illinois at Urbana-Champaign, Urbana, Illinois, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yonghua","family":"Hao","sequence":"additional","affiliation":[{"name":"Department of Pathobiology, University of Illinois at Urbana-Champaign, Urbana, Illinois, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Francis","family":"Lee","sequence":"additional","affiliation":[{"name":"Department of Pathobiology, University of Illinois at Urbana-Champaign, Urbana, Illinois, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Timothy","family":"Lee","sequence":"additional","affiliation":[{"name":"Department of Pathobiology, University of Illinois at Urbana-Champaign, Urbana, Illinois, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ryan J.","family":"Lee","sequence":"additional","affiliation":[{"name":"Department of Pathobiology, University of Illinois at Urbana-Champaign, Urbana, Illinois, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gee W.","family":"Lau","sequence":"additional","affiliation":[{"name":"Department of Pathobiology, University of Illinois at Urbana-Champaign, Urbana, Illinois, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1164\/rccm.200408-1044SO"},{"key":"e_1_3_2_3_2","first-page":"787","article-title":"The relevance of the polymicrobial nature of airway infection in the acute and chronic management of patients with cystic fibrosis","volume":"10","author":"Sibley CD","year":"2009","unstructured":"Sibley CD, Parkins MD, Rabin HR, Surette MG. 2009. 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