title: Differential activation of human neutrophils by Streptococcus mutans isolates from root surface lesions and caries-free and caries-active subjects.
abstract: Phagocytosis of bacterial pathogens is an important defense mechanism and may contribute to regulating Streptococcus mutans-induced dental caries, particularly at root surfaces. This study was undertaken to examine and compare differences in polymorphonuclear leukocyte or neutrophil activation by clinical isolates of S. mutans collected from the saliva of caries-free or caries-active individuals with S. mutans isolates from root surface lesions. S. mutans clinical isolates (5 caries-free, 5 caries-active, 5 root caries isolates and a laboratory strain) were incubated with neutrophils in the presence of normal human serum and the luminol dependent chemiluminescence was measured for 1 h at 37 degrees C. Results indicated that the caries active and laboratory strains activated neutrophils equally. The mean integration stimulated by caries-free strains, however, displayed a 25-30% enhanced neutrophil activation over the caries-active and laboratory strains. In contrast, neutrophil activation by root caries strains of S. mutans was 45-50% lower than all other S. mutans strains, possibly suggesting a natural selection for S. mutans strains that can evade neutrophil recognition and subsequent phagocytosis. Stimulation of neutrophils with the cell wall and membrane surface component preparations indicated that extracts from all four groups activated neutrophils significantly. Again, caries-free preparations activated neutrophils significantly more than caries active, laboratory strain and root caries isolates. This selection may become more important on root surfaces due to increased exposure to crevicular fluid and neutrophils. The data provide evidence for the presence or onset of mechanisms or biological alterations in S. mutans developed to circumvent neutrophil recognition and/or phagocytosis, thus increasing S. mutans survival and colonization on tooth surfaces, resulting in an enhanced risk of dental caries, particularly at root surfaces.
authors.affiliation: Department of Oral Biology, Indiana University School of Medicine, Indianapolis 46202-5186, USA.
authors.forename: M A
authors.initials: MA
authors.lastname: Moore
authors.forename: R L
authors.initials: RL
authors.lastname: Gregory
authors.forename: L M
authors.initials: LM
authors.lastname: Switalski
authors.forename: Z W
authors.initials: ZW
authors.lastname: Hakki
authors.forename: L E
authors.initials: LE
authors.lastname: Gfell
authors.forename: M J
authors.initials: MJ
authors.lastname: Kowolik
mesh_terms: D000328:Adult; D002473:Cell Wall / Q000276:immunology; D004797:Enzyme-Linked Immunosorbent Assay / Q000379:methods; D006801:Humans; D007202:Indicators and Reagents; D008163:Luminescent Measurements; D008165:Luminol; D018375:Neutrophil Activation; D010587:Phagocytosis; D017213:Root Caries / Q000276:immunology / Q000382:microbiology*; D012463:Saliva / Q000382:microbiology; D013295:Streptococcus mutans / Q000276:immunology* / Q000302:isolation & purification / Q000472:pathogenicity; D014092:Tooth Root / Q000276:immunology / Q000382:microbiology*
chemical_list: D007202:Indicators and Reagents; D008165:Luminol