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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Phylogenetic Lineage and Pilus Protein Spb1/SAN1518 Affect Opsonin-Independent Phagocytosis and Intracellular Survival of Group B Streptococcus</title><author><name sortKey="Chattopadhyay, Debasish" sort="Chattopadhyay, Debasish" uniqKey="Chattopadhyay D" first="Debasish" last="Chattopadhyay">Debasish Chattopadhyay</name><affiliation><nlm:aff id="A1">Department of Microbiology, University of Alabama at Birmingham, 845 19<sup>th</sup> Street South, BBRB 658, Birmingham AL 35294</nlm:aff></affiliation></author><author><name sortKey="Carey, Alison J" sort="Carey, Alison J" uniqKey="Carey A" first="Alison J." last="Carey">Alison J. Carey</name><affiliation><nlm:aff id="A2">School of Medical Sciences and Griffith Health Institute, Griffith University, Gold Coast QLD Australia 4222</nlm:aff></affiliation></author><author><name sortKey="Caliot, Elise" sort="Caliot, Elise" uniqKey="Caliot E" first="Elise" last="Caliot">Elise Caliot</name><affiliation><nlm:aff id="A3">Unité de Biologie des Bactéries Pathogènes à Gram Positif, Institut Pasteur, 25-28 rue du Docteur Roux, 75724 Paris Cedex 15, France</nlm:aff></affiliation></author><author><name sortKey="Webb, Richard I" sort="Webb, Richard I" uniqKey="Webb R" first="Richard I." last="Webb">Richard I. Webb</name><affiliation><nlm:aff id="A4">Centre for Microscopy and Microanalysis, University of Queensland, Australia 4072</nlm:aff></affiliation></author><author><name sortKey="Layton, James R" sort="Layton, James R" uniqKey="Layton J" first="James R." last="Layton">James R. Layton</name><affiliation><nlm:aff id="A5">Department of Medicine, University of Alabama at Birmingham, 845 19<sup>th</sup> Street South, BBRB 658, Birmingham AL 35294</nlm:aff></affiliation></author><author><name sortKey="Wang, Yan" sort="Wang, Yan" uniqKey="Wang Y" first="Yan" last="Wang">Yan Wang</name><affiliation><nlm:aff id="A6">Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis TN 38105</nlm:aff></affiliation></author><author><name sortKey="Bohnsack, John F" sort="Bohnsack, John F" uniqKey="Bohnsack J" first="John F." last="Bohnsack">John F. Bohnsack</name><affiliation><nlm:aff id="A7">Departments of Pediatrics and Pathology, University of Utah School of Medicine, Salt Lake City UT 84136</nlm:aff></affiliation></author><author><name sortKey="Adderson, Elisabeth E" sort="Adderson, Elisabeth E" uniqKey="Adderson E" first="Elisabeth E." last="Adderson">Elisabeth E. Adderson</name><affiliation><nlm:aff id="A6">Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis TN 38105</nlm:aff></affiliation></author><author><name sortKey="Ulett, Glen C" sort="Ulett, Glen C" uniqKey="Ulett G" first="Glen C." last="Ulett">Glen C. Ulett</name><affiliation><nlm:aff id="A1">Department of Microbiology, University of Alabama at Birmingham, 845 19<sup>th</sup> Street South, BBRB 658, Birmingham AL 35294</nlm:aff></affiliation><affiliation><nlm:aff id="A2">School of Medical Sciences and Griffith Health Institute, Griffith University, Gold Coast QLD Australia 4222</nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">21238599</idno><idno type="pmc">4500112</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4500112</idno><idno type="RBID">PMC:4500112</idno><idno type="doi">10.1016/j.micinf.2010.12.009</idno><date when="2011">2011</date><idno type="wicri:Area/Pmc/Corpus">001D60</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">001D60</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Phylogenetic Lineage and Pilus Protein Spb1/SAN1518 Affect Opsonin-Independent Phagocytosis and Intracellular Survival of Group B Streptococcus</title><author><name sortKey="Chattopadhyay, Debasish" sort="Chattopadhyay, Debasish" uniqKey="Chattopadhyay D" first="Debasish" last="Chattopadhyay">Debasish Chattopadhyay</name><affiliation><nlm:aff id="A1">Department of Microbiology, University of Alabama at Birmingham, 845 19<sup>th</sup> Street South, BBRB 658, Birmingham AL 35294</nlm:aff></affiliation></author><author><name sortKey="Carey, Alison J" sort="Carey, Alison J" uniqKey="Carey A" first="Alison J." last="Carey">Alison J. Carey</name><affiliation><nlm:aff id="A2">School of Medical Sciences and Griffith Health Institute, Griffith University, Gold Coast QLD Australia 4222</nlm:aff></affiliation></author><author><name sortKey="Caliot, Elise" sort="Caliot, Elise" uniqKey="Caliot E" first="Elise" last="Caliot">Elise Caliot</name><affiliation><nlm:aff id="A3">Unité de Biologie des Bactéries Pathogènes à Gram Positif, Institut Pasteur, 25-28 rue du Docteur Roux, 75724 Paris Cedex 15, France</nlm:aff></affiliation></author><author><name sortKey="Webb, Richard I" sort="Webb, Richard I" uniqKey="Webb R" first="Richard I." last="Webb">Richard I. Webb</name><affiliation><nlm:aff id="A4">Centre for Microscopy and Microanalysis, University of Queensland, Australia 4072</nlm:aff></affiliation></author><author><name sortKey="Layton, James R" sort="Layton, James R" uniqKey="Layton J" first="James R." last="Layton">James R. Layton</name><affiliation><nlm:aff id="A5">Department of Medicine, University of Alabama at Birmingham, 845 19<sup>th</sup> Street South, BBRB 658, Birmingham AL 35294</nlm:aff></affiliation></author><author><name sortKey="Wang, Yan" sort="Wang, Yan" uniqKey="Wang Y" first="Yan" last="Wang">Yan Wang</name><affiliation><nlm:aff id="A6">Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis TN 38105</nlm:aff></affiliation></author><author><name sortKey="Bohnsack, John F" sort="Bohnsack, John F" uniqKey="Bohnsack J" first="John F." last="Bohnsack">John F. Bohnsack</name><affiliation><nlm:aff id="A7">Departments of Pediatrics and Pathology, University of Utah School of Medicine, Salt Lake City UT 84136</nlm:aff></affiliation></author><author><name sortKey="Adderson, Elisabeth E" sort="Adderson, Elisabeth E" uniqKey="Adderson E" first="Elisabeth E." last="Adderson">Elisabeth E. Adderson</name><affiliation><nlm:aff id="A6">Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis TN 38105</nlm:aff></affiliation></author><author><name sortKey="Ulett, Glen C" sort="Ulett, Glen C" uniqKey="Ulett G" first="Glen C." last="Ulett">Glen C. Ulett</name><affiliation><nlm:aff id="A1">Department of Microbiology, University of Alabama at Birmingham, 845 19<sup>th</sup> Street South, BBRB 658, Birmingham AL 35294</nlm:aff></affiliation><affiliation><nlm:aff id="A2">School of Medical Sciences and Griffith Health Institute, Griffith University, Gold Coast QLD Australia 4222</nlm:aff></affiliation></author></analytic><series><title level="j">Microbes and infection / Institut Pasteur</title><idno type="ISSN">1286-4579</idno><idno type="eISSN">1769-714X</idno><imprint><date when="2011">2011</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p id="P1">Opsonin-independent phagocytosis of Group B Streptococcus (GBS) is important in defense against neonatal GBS infections. A recent study indicated a role for GBS pilus in macrophage phagocytosis. We studied 163 isolates from different phylogenetic backgrounds and those possessing or lacking the gene encoding the pilus backbone protein, Spb1 (SAN1518, PI-2b) and <italic>spb1</italic>-deficient mutants of wild-type (WT) serotype III-3 GBS 874391 in non-opsonic phagocytosis assays using J774A.1 macrophages. Numbers of GBS phagocytosed differed up to 23-fold depending on phylogenetic background; isolates possessing <italic>spb1</italic> were phagocytosed more than isolates lacking <italic>spb1</italic>. Comparing WT GBS and isogenic <italic>spb1</italic>-deficient mutants showed WT was phagocytosed better compared to mutants; Spb1 also enhanced intracellular survival as mutants were killed more efficiently. Complementation of mutants restored phagocytosis and resistance to killing in J774A.1 macrophages. Spb1 antiserum revealed surface expression in WT GBS and spatial distribution relative to capsular polysaccharide. <italic>spb1</italic> did not affect macrophage nitric oxide and TNF-alpha responses; differences in phagocytosis did not correlate with N-acetyl D-glucosamine (from GBS cell wall) according to enzyme-linked lectin-sorbent assay. Together, these findings support a role for phylogenetic lineage and Spb1 in opsonin-independent phagocytosis and intracellular survival of GBS in J774A.1 macrophages.</p></div></front></TEI><pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<pmc-dir>properties manuscript</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-journal-id">100883508</journal-id><journal-id journal-id-type="pubmed-jr-id">21592</journal-id><journal-id journal-id-type="nlm-ta">Microbes Infect</journal-id><journal-id journal-id-type="iso-abbrev">Microbes Infect.</journal-id><journal-title-group><journal-title>Microbes and infection / Institut Pasteur</journal-title></journal-title-group><issn pub-type="ppub">1286-4579</issn><issn pub-type="epub">1769-714X</issn></journal-meta><article-meta><article-id pub-id-type="pmid">21238599</article-id><article-id pub-id-type="pmc">4500112</article-id><article-id pub-id-type="doi">10.1016/j.micinf.2010.12.009</article-id><article-id pub-id-type="manuscript">NIHMS703549</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>Phylogenetic Lineage and Pilus Protein Spb1/SAN1518 Affect Opsonin-Independent Phagocytosis and Intracellular Survival of Group B Streptococcus</article-title></title-group><contrib-group><contrib contrib-type="author" equal-contrib="yes"><name><surname>Chattopadhyay</surname><given-names>Debasish</given-names></name><xref ref-type="aff" rid="A1">a</xref></contrib><contrib contrib-type="author" equal-contrib="yes"><name><surname>Carey</surname><given-names>Alison J.</given-names></name><xref ref-type="aff" rid="A2">b</xref></contrib><contrib contrib-type="author"><name><surname>Caliot</surname><given-names>Elise</given-names></name><xref ref-type="aff" rid="A3">c</xref></contrib><contrib contrib-type="author"><name><surname>Webb</surname><given-names>Richard I.</given-names></name><xref ref-type="aff" rid="A4">d</xref></contrib><contrib contrib-type="author"><name><surname>Layton</surname><given-names>James R.</given-names></name><xref ref-type="aff" rid="A5">e</xref></contrib><contrib contrib-type="author"><name><surname>Wang</surname><given-names>Yan</given-names></name><xref ref-type="aff" rid="A6">f</xref></contrib><contrib contrib-type="author"><name><surname>Bohnsack</surname><given-names>John F.</given-names></name><xref ref-type="aff" rid="A7">g</xref></contrib><contrib contrib-type="author"><name><surname>Adderson</surname><given-names>Elisabeth E.</given-names></name><xref ref-type="aff" rid="A6">f</xref></contrib><contrib contrib-type="author"><name><surname>Ulett</surname><given-names>Glen C.</given-names></name><xref ref-type="aff" rid="A1">a</xref><xref ref-type="aff" rid="A2">b</xref><xref ref-type="corresp" rid="CR1">*</xref></contrib></contrib-group><aff id="A1"><label>a</label>Department of Microbiology, University of Alabama at Birmingham, 845 19<sup>th</sup> Street South, BBRB 658, Birmingham AL 35294</aff><aff id="A2"><label>b</label>School of Medical Sciences and Griffith Health Institute, Griffith University, Gold Coast QLD Australia 4222</aff><aff id="A3"><label>c</label>Unité de Biologie des Bactéries Pathogènes à Gram Positif, Institut Pasteur, 25-28 rue du Docteur Roux, 75724 Paris Cedex 15, France</aff><aff id="A4"><label>d</label>Centre for Microscopy and Microanalysis, University of Queensland, Australia 4072</aff><aff id="A5"><label>e</label>Department of Medicine, University of Alabama at Birmingham, 845 19<sup>th</sup> Street South, BBRB 658, Birmingham AL 35294</aff><aff id="A6"><label>f</label>Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis TN 38105</aff><aff id="A7"><label>g</label>Departments of Pediatrics and Pathology, University of Utah School of Medicine, Salt Lake City UT 84136</aff><author-notes><corresp id="CR1"><label>*</label> Correspondence: Glen C Ulett, School of Medical Sciences and Griffith Health Institute, Griffith University, Gold Coast QLD Australia 4222; Ph: 61 7 5678 0765 Fax: 61 7 5678 0795 <email>g.ulett@griffith.edu.au</email></corresp></author-notes><pub-date pub-type="nihms-submitted"><day>28</day><month>6</month><year>2015</year></pub-date><pub-date pub-type="epub"><day>14</day><month>1</month><year>2011</year></pub-date><pub-date pub-type="ppub"><month>4</month><year>2011</year></pub-date><pub-date pub-type="pmc-release"><day>13</day><month>7</month><year>2015</year></pub-date><volume>13</volume><issue>4</issue><fpage>369</fpage><lpage>382</lpage><pmc-comment>elocation-id from pubmed: 10.1016/j.micinf.2010.12.009</pmc-comment>
<abstract><p id="P1">Opsonin-independent phagocytosis of Group B Streptococcus (GBS) is important in defense against neonatal GBS infections. A recent study indicated a role for GBS pilus in macrophage phagocytosis. We studied 163 isolates from different phylogenetic backgrounds and those possessing or lacking the gene encoding the pilus backbone protein, Spb1 (SAN1518, PI-2b) and <italic>spb1</italic>-deficient mutants of wild-type (WT) serotype III-3 GBS 874391 in non-opsonic phagocytosis assays using J774A.1 macrophages. Numbers of GBS phagocytosed differed up to 23-fold depending on phylogenetic background; isolates possessing <italic>spb1</italic> were phagocytosed more than isolates lacking <italic>spb1</italic>. Comparing WT GBS and isogenic <italic>spb1</italic>-deficient mutants showed WT was phagocytosed better compared to mutants; Spb1 also enhanced intracellular survival as mutants were killed more efficiently. Complementation of mutants restored phagocytosis and resistance to killing in J774A.1 macrophages. Spb1 antiserum revealed surface expression in WT GBS and spatial distribution relative to capsular polysaccharide. <italic>spb1</italic> did not affect macrophage nitric oxide and TNF-alpha responses; differences in phagocytosis did not correlate with N-acetyl D-glucosamine (from GBS cell wall) according to enzyme-linked lectin-sorbent assay. Together, these findings support a role for phylogenetic lineage and Spb1 in opsonin-independent phagocytosis and intracellular survival of GBS in J774A.1 macrophages.</p></abstract><kwd-group><kwd>GROUP B STREPTOCOCCUS</kwd><kwd><italic>STREPTOCOCCUS AGALACTIAE</italic></kwd><kwd>MACROPHAGE</kwd><kwd>PHAGOCYTOSIS</kwd><kwd>PILUS</kwd><kwd>INTRACELLULAR SURVIVAL</kwd></kwd-group></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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