Analysis of Mechanism for Specific Immune Response Induction to Periodontopathic Bacteria

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Primary immune responses are initiated by dendritic cells (DC), which inform naive Th cells about invading pathogens. DC settle as interstitial DC and Langerhans cells in peripheral non-lymphoid tissues including gingiva. These peripheral DC capture and process Ag at the site of inflammation, and then migrate to lymph nodes to prime Th cells. DC undergo a series of events leading to irreversible maturation upon stimulation with invading bacteria, and up-regulate cytokine production and surface molecule expression with different kinetics. To investigate the responses DC during periodontal infection, we analyzed(1)the sensitivitly to Human Leukocyte Elastase (HLE) digestion of CD40 on DC,(2)the effects of LPS and fimbriae from P. gingivalis on the phenotype of human in DC. CD40 on DC was resistant to HLE treatment, unlike the molecule of human gingival fibroblasts, suggesting that DC were capale to stimulate the local immune responses after PMNL infiltration. Furthermore, P. gingivalis L … More PS and fimbriae preferentially up-regulated CD14 and CD16 expression on immature PBDC (CD14^-CD16^-), although E. coli LPS did not alter the expression of these molecules. P. gingivalis LPS-induced CD14^+CD16^+ cells strongly expressed dendritic cell markers: Cdla and HLA-DR, and CD54 was highly expressed. However, CD40, CD80, CD83, CD86 expression was lower than E.coli LPS-stimulated DC, suggesting these cells were in DC with weak immunnostimulatory activity. P.gingivalis LPS was a weaker stimulator in terms of IL-6, IL-8, IL-10, IL-12, and RANTES production from DC as compared to E.coli LPS. Both LPS stimulated-DC induced comparable up-take of dextran-FITC, although P.gingivalis induced the statistically weaker allogenic T cell proliferation. These results suggestively indicated P. gingivalis LPS and fimbriae trigger a maturation of DC with unique characteristics, that modulate immune responses occurred at the site of periodontal infection. P.gingivalis-induced CD14^+CD16^+DC subsets may contribute to induction of chronic inflammation. Less