Phylogenetic lineage and pilus protein Spb1/SAN1518 affect opsonin-independent phagocytosis and intracellular survival of Group B Streptococcus.
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 (Maisey et al Faseb J 22 2008 1715-24). 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 spb1-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 spb1 were phagocytosed more than isolates lacking spb1. Comparing WT GBS and isogenic spb1-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. spb1 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.
Department of Microbiology, University of Alabama at Birmingham, 845 19 Street South, BBRB 658, Birmingham AL 35294.
Debasish
D
Chattopadhyay
School of Medical Sciences and Griffith Health Institute, Griffith University, Gold Coast QLD Australia 4222.
Alison J
AJ
Carey
Unité de Biologie des Bactéries Pathogènes à Gram Positif, Institut Pasteur, 25-28 rue du Docteur Roux, 75724 Paris Cedex 15, France.
Elise
E
Caliot
Centre for Microscopy and Microanalysis, University of Queensland, Australia 4072.
Richard I
RI
Webb
Department of Medicine, University of Alabama at Birmingham, 845 19 Street South, BBRB 658, Birmingham AL 35294.
James R
JR
Layton
Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis TN 38105.
Yan
Y
Wang
Departments of Pediatrics and Pathology, University of Utah School of Medicine, Salt Lake City UT 84136.
John F
JF
Bohnsack
Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis TN 38105.
Elisabeth E
EE
Adderson
Department of Microbiology, University of Alabama at Birmingham, 845 19 Street South, BBRB 658, Birmingham AL 35294.|School of Medical Sciences and Griffith Health Institute, Griffith University, Gold Coast QLD Australia 4222.
Glen C
GC
Ulett
D000117:Acetylglucosamine / Q000276:immunology; D000818:Animals; D001426:Bacterial Proteins / Q000235:genetics / Q000378:metabolism*; D002460:Cell Line; D015964:Gene Expression Regulation, Bacterial; D006801:Humans; D042541:Intracellular Space / Q000276:immunology; D008262:Macrophage Activation / Q000276:immunology; D008264:Macrophages / Q000276:immunology; D008565:Membrane Proteins / Q000235:genetics / Q000378:metabolism*; D051379:Mice; D050296:Microbial Viability / Q000276:immunology; D009895:Opsonin Proteins / Q000276:immunology; D010587:Phagocytosis; D010802:Phylogeny; D021381:Protein Transport; D013290:Streptococcal Infections / Q000276:immunology* / Q000382:microbiology*; D013292:Streptococcus agalactiae / Q000235:genetics / Q000276:immunology / Q000502:physiology*; D020298:U937 Cells
D001426:Bacterial Proteins; D008565:Membrane Proteins; D009895:Opsonin Proteins; C480220:Spb1 protein, Streptococcus agalactiae; D000117:Acetylglucosamine
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