4.5 Article

Expression of cytokines and inducible nitric oxide synthase in inflamed gingival tissue

期刊

JOURNAL OF PERIODONTOLOGY
卷 72, 期 5, 页码 590-597

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AMER ACAD PERIODONTOLOGY
DOI: 10.1902/jop.2001.72.5.590

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Actinobacillus actinomycetemcomitans; Porphyromonas gingivalis; periodontal diseases/microbiology; cytokines; nitric oxide synthase; polymerase chain reaction; reverse transcription

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Background: Periodontopathic bacteria induce inflammation of periodontal tissues. The cytokines and nitric oxide released in periodontal lesions have been reported to play a protective role in bacterial infection and to relate to the process of inflammation. To clarify the relationship between colonization of periodontopathic bacteria and cytokines, we evaluated profiles of inflammatory cytokines, chemokine, anti-inflammatory cytokines, and inducible nitric oxide synthase (iNOS) and colonization by Porphyromonas gingivalis and Actinobacillus actinomycetemcomitans, which are major pathogens of periodontitis. Methods: mRNA expression of cytokines and iNOS in inflamed and healthy gingival tissue was determined using reverse transcription-polymerase chain reaction (RT-PCR), and the relationship between their profiles and the detection of specific bacteria was analyzed. Results: The relative expression of interleukin (IL)-6 and iNOS mRNAs in periodontal lesions was significantly higher than those in healthy individuals. IL-6 mRNA expression was also significantly higher at bleeding on probing (BOP)-positive sites than at BOP-negative sites. The expressions of IL-1 alpha and IL-8 increased, but IL-IO expression decreased at sites where A. actinomycetemcomitans was detected. We found no correlation between the expression of cytokine and iNOS mRNA and infection by P. gingivalis. Conclusions: The expression of IL-6 may reflect inflammation in gingival tissue, and iNOS may be involved in the inflammatory process in periodontitis. The presence of A. actinomycetemcomitans or P. gingivalis might relate to the different cytokine profiles of IL-1 alpha, IL-8, and IL-10.

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