4.6 Article

Ability of oral bacteria to induce tissue-destructive molecules from human neutrophils

期刊

ORAL DISEASES
卷 14, 期 4, 页码 327-334

出版社

WILEY
DOI: 10.1111/j.1601-0825.2007.01382.x

关键词

neutrophils; oral bacteria; phagocytosis; tissue-destructive molecules

资金

  1. National Research Foundation of Korea [전06A1202, 2003-041-E00255] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)

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AIM: The induction of tissue-destructive molecules from neutrophils by periodontopathic bacteria has been suggested as one of the mechanisms of periodontal destruction. The aim of this study was to determine whether the ability to stimulate neutrophils is an authentic characteristic of periodontopathic bacteria. METHODS: We evaluated, along with phagocytosis, the production of reactive oxygen species (ROS), matrix metalloproteinase-8 (MMP-8), and interleukin-1 beta by neutrophils in response to non-periodontopathic Streptococcus sanguinis and periodontopathic bacteria Fusobacterium nucleatum and Treponema denticola, in the absence or presence of antibodies. Phagocytosis, the death of neutrophils, and intracellular ROS production were measured by flow cytometry and the concentrations of MMP-8 and interleukin-1 beta secreted into medium were determined by enzyme-linked immunosorbent assay. RESULTS: S. sanguinis and F. nucleatum induced greater production of ROS, MMP-8, and interleukin-1 beta than did T. denticola. The levels of tissue-destructive molecules produced by neutrophils had a positive correlation with phagocytosis. Opsonization of bacteria with antibodies significantly increased phagocytosis and ROS production and release, thus increasing both bacterial clearance and potential tissue damage. CONCLUSION: The ability of oral bacteria to induce tissue-destructive molecules from neutrophils is not an inherent characteristic of periodontopathic bacteria, which would provide a new insight into the role of neutrophils in periodontal destruction.

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