Oral microbiology and immunology · 2009
Toll-like receptors 2 and 5 in human gingival epithelial cells co-operate with T-cell cytokine interleukin-17.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Beklen A, Sorsa T, Konttinen Y T
Аннотация
BACKGROUND/AIM: Periodontitis begins as the result of perturbation of the gingival epithelial cells caused by subgingival bacteria interacting with the epithelial cells via pattern recognition receptors. Toll-like receptors (TLRs) have been shown to play an important role in the recognition of periodontal pathogens so we have studied the interaction of TLR ligands with TLR2 and TLR5 for cytokine production in the cultures of gingival epithelial cells.
METHODS: Immunohistochemistry was used for the localization of TLR2 and TLR5 in tissue specimens. Enzyme-linked immunosorbent assays were performed to detect the levels of interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha), released from gingival epithelial cell cultures following stimulation with TLR ligand alone or in combination with IL-17.
RESULTS: Both TLR2 and TLR5 were increased in periodontitis (2128 +/- 159 vs. 449 +/- 59 and 2456 +/- 297 vs. 679 +/- 103, respectively, P < 0.001) including gingival epithelial cells that stained strongly. Cultured gingival epithelial cells stimulated with their respective ligands (HKLM, a TLR2 ligand that is also found in Porphyromonas gingivalis, and flagellin, a TLR5 ligand that is also found in Treponema denticola) produced both IL-1beta and TNF-alpha. To mimic T-cell help, IL-17 was added. This further greatly enhanced TLR ligand-induced IL-1beta (P < 0.001) and TNF-alpha (P < 0.01) production.
CONCLUSIONS: These findings show how pathogen-associated molecular patterns, shared by many different periodontopathogenic bacteria, stimulate the resident gingival epithelial cells to inflammatory responses in a TLR-dependent manner. This stimulation may be particularly strong in periodontitis and when T helper type 17 cells provide T-cell help in intercellular cooperation.
METHODS: Immunohistochemistry was used for the localization of TLR2 and TLR5 in tissue specimens. Enzyme-linked immunosorbent assays were performed to detect the levels of interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha), released from gingival epithelial cell cultures following stimulation with TLR ligand alone or in combination with IL-17.
RESULTS: Both TLR2 and TLR5 were increased in periodontitis (2128 +/- 159 vs. 449 +/- 59 and 2456 +/- 297 vs. 679 +/- 103, respectively, P < 0.001) including gingival epithelial cells that stained strongly. Cultured gingival epithelial cells stimulated with their respective ligands (HKLM, a TLR2 ligand that is also found in Porphyromonas gingivalis, and flagellin, a TLR5 ligand that is also found in Treponema denticola) produced both IL-1beta and TNF-alpha. To mimic T-cell help, IL-17 was added. This further greatly enhanced TLR ligand-induced IL-1beta (P < 0.001) and TNF-alpha (P < 0.01) production.
CONCLUSIONS: These findings show how pathogen-associated molecular patterns, shared by many different periodontopathogenic bacteria, stimulate the resident gingival epithelial cells to inflammatory responses in a TLR-dependent manner. This stimulation may be particularly strong in periodontitis and when T helper type 17 cells provide T-cell help in intercellular cooperation.