title: Effect of salivary agglutination on oral streptococcal clearance by human polymorphonuclear neutrophil granulocytes.
abstract: Salivary agglutination is an important host defense mechanism to aggregate oral commensal bacteria as well as invading pathogens. Saliva flow and subsequent swallowing more easily clear aggregated bacteria compared with single cells. Phagocytic clearance of bacteria through polymorphonuclear neutrophil granulocytes also seems to increase to a certain extent with the size of bacterial aggregates. To determine a connection between salivary agglutination and the host innate immune response by phagocytosis, an in vitro agglutination assay was developed reproducing the average size of salivary bacterial aggregates. Using the oral commensal Streptococcus gordonii as a model organism, the effect of salivary agglutination on phagocytic clearance through polymorphonuclear neutrophil granulocytes was investigated. Here we describe how salivary aggregates of S. gordonii are readily cleared through phagocytosis, whereas single bacterial cells showed a significant delay in being phagocytosed and killed. Furthermore, before phagocytosis the polymorphonuclear neutrophil granulocytes were able to induce a specific de-aggregation, which was dependent on serine protease activity. The data presented suggest that salivary agglutination of bacterial cells leads to an ideal size for recognition by polymorphonuclear neutrophil granulocytes. As a first line of defense, these phagocytic cells are able to recognize the aggregates and de-aggregate them via serine proteases to a more manageable size for efficient phagocytosis and subsequent killing in the phagolysosome. This observed mechanism not only prevents the rapid spreading of oral bacterial cells while entering the bloodstream but would also avoid degranulation of involved polymorphonuclear neutrophil granulocytes, so preventing collateral damage to nearby tissue.
authors.affiliation: Department of Microbiology and Immunology, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA.
authors.forename: A
authors.initials: A
authors.lastname: Itzek
authors.affiliation: Department of Microbiology and Immunology, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA.
authors.forename: Z
authors.initials: Z
authors.lastname: Chen
authors.affiliation: Department of Restorative Dentistry, Oregon Health and Science University, Portland, OR, USA.
authors.forename: J
authors.initials: J
authors.lastname: Merritt
authors.affiliation: Department of Restorative Dentistry, Oregon Health and Science University, Portland, OR, USA.
authors.forename: J
authors.initials: J
authors.lastname: Kreth
mesh_terms: D000371:Agglutination; D006801:Humans; D007113:Immunity, Innate; D009055:Mouth / Q000276:immunology / Q000382:microbiology*; D009504:Neutrophils / Q000276:immunology*; D010587:Phagocytosis; D012463:Saliva / Q000502:physiology*; D057057:Serine Proteases / Q000378:metabolism; D054773:Streptococcus gordonii / Q000276:immunology* / Q000502:physiology
chemical_list: D057057:Serine Proteases
keywords: 
  Streptococcus gordonii
  ; innate immunity; polymorphonuclear neutrophil granulocytes; salivary agglutination