title: Effects of herpes simplex virus type 1 infection on immune functions of human neutrophils.
abstract: OBJECTIVE
  Herpesviruses may play roles in the development of periodontal diseases. This study analyzed the effects of herpes simplex virus type 1 (HSV-1) infection on neutrophil function. The effects of lipopolysaccharide (LPS) from the periodontal pathogen, Porphyromonas gingivalis, during HSV-1 infection were also determined.
  
  
  METHODS
  Purified HSV-1 was pretreated with buffer containing no serum, with HSV-1 immunoglobulin G (IgG)-positive serum (HSV-1 antiserum) or with control serum. Neutrophils were mock-infected or infected with the pretreated HSV-1. Viral binding and phagosome formation were detected using immunostaining. Intracellular reactive oxygen species (ROS) were determined using 2',7'-dichlorofluorescin diacetate and fluorometry. Leukotriene B(4) (LTB(4)) and interleukin-8 (IL-8) were detected using enzyme immunoassays. Release of matrix metalloproteinase-9 (MMP-9) was examined using gelatin zymography. Phosphorylation of Akt/glycogen synthase kinase-3 (GSK-3) was determined using western blotting.
  
  
  RESULTS
  HSV-1 bound directly to neutrophils and enhanced the release of MMP-9. HSV-1 immune complexes, formed in the HSV-1 antiserum, bound neutrophils and induced the formation of early phagosome more effectively than did HSV-1 alone. The relative levels of ROS and phosphorylation of Akt/GSK-3 were increased significantly in neutrophils after infection with HSV-1 immune complexes. Infection with HSV-1 and HSV-1 immune complexes also stimulated the production of inflammatory mediators, LTB(4) and IL-8. Moreover, LPS enhanced the HSV-1-stimulatory production of IL-8.
  
  
  CONCLUSIONS
  This study demonstrated differences in neutrophils infected with HSV-1 alone or with HSV-1 immune complexes, suggesting that opsonization of HSV-1 might enhance its effects on neutrophils. The in vitro findings suggest that HSV-1 infection may induce the inflammatory response and affect periodontal health.
authors.affiliation: Institute of Oral Biology, National Yang-Ming University, Taipei, Taiwan.
authors.forename: S-L
authors.initials: SL
authors.lastname: Hung
authors.forename: H-H
authors.initials: HH
authors.lastname: Chiang
authors.forename: C-Y
authors.initials: CY
authors.lastname: Wu
authors.forename: M-J
authors.initials: MJ
authors.lastname: Hsu
authors.forename: Y-T
authors.initials: YT
authors.lastname: Chen
mesh_terms: D000914:Antibodies, Viral / Q000276:immunology; D000936:Antigen-Antibody Complex / Q000276:immunology; D005260:Female; D005452:Fluoresceins; D005456:Fluorescent Dyes; D005470:Fluorometry; D038362:Glycogen Synthase Kinase 3 / Q000032:analysis; D018259:Herpesvirus 1, Human / Q000276:immunology*; D006801:Humans; D007106:Immune Sera / Q000276:immunology; D007074:Immunoglobulin G / Q000276:immunology; D018836:Inflammation Mediators / Q000032:analysis; D016209:Interleukin-8 / Q000032:analysis; D007975:Leukotriene B4 / Q000032:analysis; D008070:Lipopolysaccharides / Q000494:pharmacology; D008297:Male; D020780:Matrix Metalloproteinase 9 / Q000032:analysis; D009504:Neutrophils / Q000187:drug effects / Q000201:enzymology / Q000276:immunology*; D051058:Oncogene Protein v-akt / Q000032:analysis; D010588:Phagosomes / Q000821:virology; D016966:Porphyromonas gingivalis; D017382:Reactive Oxygen Species / Q000032:analysis; D013283:Stomatitis, Herpetic / Q000276:immunology*; D053585:Virus Attachment; D055815:Young Adult
chemical_list: D000914:Antibodies, Viral; D000936:Antigen-Antibody Complex; D005452:Fluoresceins; D005456:Fluorescent Dyes; D007106:Immune Sera; D007074:Immunoglobulin G; D018836:Inflammation Mediators; D016209:Interleukin-8; D008070:Lipopolysaccharides; D017382:Reactive Oxygen Species; D007975:Leukotriene B4; C029569:diacetyldichlorofluorescein; D051058:Oncogene Protein v-akt; D038362:Glycogen Synthase Kinase 3; D020780:Matrix Metalloproteinase 9