{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,9]],"date-time":"2026-10-09T07:52:15Z","timestamp":1791532335458,"version":"4.3.4"},"reference-count":29,"publisher":"National Academy of Sciences","issue":"40","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2004,10,5]]},"abstract":"<jats:p>\n                    Group B\n                    <jats:italic>Streptococcus<\/jats:italic>\n                    (GBS) is a major cause of pneumonia, bacteremia, and meningitis in neonates and has been found to persist inside host phagocytic cells. The pore-forming GBS \u03b2-hemolysin\/cytolysin (\u03b2H\/C) encoded by\n                    <jats:italic>cylE<\/jats:italic>\n                    is an important virulence factor as demonstrated in several\n                    <jats:italic>in vivo<\/jats:italic>\n                    models. Interestingly,\n                    <jats:italic>cylE<\/jats:italic>\n                    deletion results not only in the loss of \u03b2H\/C activity, but also in the loss of a carotenoid pigment of unknown function. In this study, we sought to define the mechanism(s) by which\n                    <jats:italic>cylE<\/jats:italic>\n                    may contribute to GBS phagocyte resistance and increased virulence potential. We found that\n                    <jats:italic>cylE<\/jats:italic>\n                    -deficient GBS was more readily cleared from a mouse's bloodstream, human whole blood, and isolated macrophage and neutrophil cultures. Survival was linked to the ability of \u03b2H\/C to induce cytolysis and apoptosis of the phagocytes. At a lower bacterial inoculum,\n                    <jats:italic>cylE<\/jats:italic>\n                    also contributed to enhanced survival within phagocytes that was attributed to the ability of carotenoid to shield GBS from oxidative damage. In oxidant killing assays,\n                    <jats:italic>cylE<\/jats:italic>\n                    mutants were shown to be more susceptible to hydrogen peroxide, hypochlorite, superoxide, and singlet oxygen. Together, these data suggest a mechanism by which the linked\n                    <jats:italic>cylE<\/jats:italic>\n                    -encoded phenotypes, \u03b2H\/C (sword) and carotenoid (shield), act in partnership to thwart the immune phagocytic defenses.\n                  <\/jats:p>","DOI":"10.1073\/pnas.0406143101","type":"journal-article","created":{"date-parts":[[2004,9,20]],"date-time":"2004-09-20T20:25:03Z","timestamp":1095711903000},"page":"14491-14496","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":205,"title":["Sword and shield: Linked group B streptococcal \u03b2-hemolysin\/cytolysin and carotenoid pigment function to subvert host phagocyte defense"],"prefix":"10.1073","volume":"101","author":[{"given":"George Y.","family":"Liu","sequence":"first","affiliation":[{"name":"Departments of Pediatrics and Pharmacology and Center for Marine Biotechnology and Biomedicine, The Scripps Institution of Oceanography, University of California at San Diego, La Jolla, CA 92093; and Microbiology Section, Department of Experimental Medicine and Biochemical Sciences, University of Perugia, 06122 Perugia, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kelly S.","family":"Doran","sequence":"additional","affiliation":[{"name":"Departments of Pediatrics and Pharmacology and Center for Marine Biotechnology and Biomedicine, The Scripps Institution of Oceanography, University of California at San Diego, La Jolla, CA 92093; and Microbiology Section, Department of Experimental Medicine and Biochemical Sciences, University of Perugia, 06122 Perugia, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Toby","family":"Lawrence","sequence":"additional","affiliation":[{"name":"Departments of Pediatrics and Pharmacology and Center for Marine Biotechnology and Biomedicine, The Scripps Institution of Oceanography, University of California at San Diego, La Jolla, CA 92093; and Microbiology Section, Department of Experimental Medicine and Biochemical Sciences, University of Perugia, 06122 Perugia, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nicole","family":"Turkson","sequence":"additional","affiliation":[{"name":"Departments of Pediatrics and Pharmacology and Center for Marine Biotechnology and Biomedicine, The Scripps Institution of Oceanography, University of California at San Diego, La Jolla, CA 92093; and Microbiology Section, Department of Experimental Medicine and Biochemical Sciences, University of Perugia, 06122 Perugia, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Manuela","family":"Puliti","sequence":"additional","affiliation":[{"name":"Departments of Pediatrics and Pharmacology and Center for Marine Biotechnology and Biomedicine, The Scripps Institution of Oceanography, University of California at San Diego, La Jolla, CA 92093; and Microbiology Section, Department of Experimental Medicine and Biochemical Sciences, University of Perugia, 06122 Perugia, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Luciana","family":"Tissi","sequence":"additional","affiliation":[{"name":"Departments of Pediatrics and Pharmacology and Center for Marine Biotechnology and Biomedicine, The Scripps Institution of Oceanography, University of California at San Diego, La Jolla, CA 92093; and Microbiology Section, Department of Experimental Medicine and Biochemical Sciences, University of Perugia, 06122 Perugia, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Victor","family":"Nizet","sequence":"additional","affiliation":[{"name":"Departments of Pediatrics and Pharmacology and Center for Marine Biotechnology and Biomedicine, The Scripps Institution of Oceanography, University of California at San Diego, La Jolla, CA 92093; 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