Bartold P M, Narayanan A S, Page R C
Department of Pathology, University of Adelaide, South Australia.
J Periodontal Res. 1992 Sep;27(5):499-505. doi: 10.1111/j.1600-0765.1992.tb01823.x.
Lipopolysaccharide from a variety of bacterial sources is known to inhibit gingival fibroblast proliferation and synthetic activity and has been implicated in the pathogenesis of periodontal inflammation. However, it may be involved not only in pathogenesis but also be responsible for delayed wound healing following periodontal therapy. The aim of this investigation was to determine whether the inhibitory effect of LPS on gingival fibroblast proliferation could be reversed by growth factors. Human gingival fibroblasts were cultured in the presence of varying concentrations of platelet-derived growth factor (PDGF) or Salmonella enteritidis LPS to determine the optimal concentrations for stimulation and inhibition of proliferation respectively. The effect of PDGF on LPS inhibition of fibroblast proliferation was studied by combining PDGF and LPS together at the outset of the experimental period or adding PDGF to cells which had been previously primed with LPS. Cell proliferation was monitored by incorporation of 3H-thymidine into precipitable DNA. The results indicated that maximal inhibition of fibroblast proliferation was obtained with 50 micrograms/ml LPS and maximal stimulation of proliferation with 5 ng/ml PDGF. PDGF was found to restore the proliferative activity of the cells exposed to LPS to approximately 60% of their control counterparts. A similar value was obtained for cultures exposed to PDGF after an extended priming period of LPS exposure. Subtle differences were noted in the time taken for cells to complete their cell cycle in the various culture conditions and this may reflect variations in subpopulations of cells in their response to various mitogenic stimuli. Overall the results indicate that PDGF has the capacity to significantly negate and reverse the inhibitory effects of LPS on human gingival fibroblast proliferation.
已知来自多种细菌来源的脂多糖可抑制牙龈成纤维细胞的增殖和合成活性，并与牙周炎症的发病机制有关。然而，它可能不仅参与发病机制，还可能是牙周治疗后伤口愈合延迟的原因。本研究的目的是确定生长因子是否能逆转脂多糖对牙龈成纤维细胞增殖的抑制作用。将人牙龈成纤维细胞在不同浓度的血小板衍生生长因子（PDGF）或肠炎沙门氏菌脂多糖存在下培养，以分别确定刺激和抑制增殖的最佳浓度。通过在实验开始时将PDGF和脂多糖联合使用，或向预先用脂多糖预处理的细胞中添加PDGF，研究PDGF对脂多糖抑制成纤维细胞增殖的影响。通过将3H-胸腺嘧啶掺入可沉淀的DNA中来监测细胞增殖。结果表明，50微克/毫升的脂多糖可最大程度地抑制成纤维细胞增殖，5纳克/毫升的PDGF可最大程度地刺激增殖。发现PDGF可将暴露于脂多糖的细胞的增殖活性恢复至其对照细胞的约60%。对于在延长的脂多糖暴露预处理期后暴露于PDGF的培养物，也获得了类似的值。在不同培养条件下，细胞完成其细胞周期所需的时间存在细微差异，这可能反映了细胞亚群对各种促有丝分裂刺激反应的差异。总体而言，结果表明PDGF有能力显著抵消并逆转脂多糖对人牙龈成纤维细胞增殖的抑制作用。
