Hill S J, Ebersole J L
Department of Periodontics and Microbiology, University of Texas Health Science Center at San Antonio, USA.
J Periodontol. 1996 Dec;67(12):1274-80. doi: 10.1902/jop.1996.67.12.1274.
Quiescent and non-quiescent human gingival fibroblasts (HGF) were incubated for 24 hours with Actinobacillus actinomycetemcomitans lipopolysaccharide (LPS) and/or growth factors (interleukin-1 beta [IL-1 beta], insulin, epidermal growth factor [EGF], platelet-derived growth factor [PDGF], fibroblast growth factor [FGF], and transforming growth factor-beta [TGF-beta]) to examine the ability of LPS to modify HGF proliferation in response to these autocrine and paracrine growth factors. A. actinomycetemcomitans LPS at high concentrations (> or = 9 micrograms/well) generally resulted in a reduction in DNA synthesis in quiescent and non-quiescent fibroblasts; however, LPS at low concentrations (< 9 micrograms/well) showed a minimal enhancement of DNA synthesis (40 to 60%) in quiescent and non-quiescent cells. HGF co-incubated with mitogenic agents and LPS (9 micrograms/well) exhibited suppression of growth factor-induced 3H-Tdr uptake compared to growth factor-stimulated controls. In contrast, 3H-Tdr uptake was slightly elevated with addition of LPS at low concentrations (0.09 microgram/well). These trends were seen with all growth factors tested. Non-quiescent cells, in general, were more responsive to the growth factors and LPS/growth factor combinations when compared to the quiescent HGF. HGF were further tested for the ability of LPS to alter growth factor responsiveness by pretreating the cells with LPS prior to incubation of the growth factor, as well as, subsequent addition of LPS to growth factor-pretreated cells. Similar patterns were observed as above, except IL-1 beta-pretreated quiescent and non-quiescent HGF followed by LPS addition demonstrated a marked elevation in proliferation when compared to IL-1 beta stimulated controls. These findings suggest that LPS may potentially modulate the proliferative rate of connective tissue undergoing inflammatory or growth factor-induced reparative processes in periodontal lesions.
将静止和非静止的人牙龈成纤维细胞（HGF）与伴放线放线杆菌脂多糖（LPS）和/或生长因子（白细胞介素-1β [IL-1β]、胰岛素、表皮生长因子 [EGF]、血小板衍生生长因子 [PDGF]、成纤维细胞生长因子 [FGF] 和转化生长因子-β [TGF-β]）一起孵育24小时，以研究LPS改变HGF对这些自分泌和旁分泌生长因子反应的增殖能力。高浓度（≥9微克/孔）的伴放线放线杆菌LPS通常会导致静止和非静止成纤维细胞的DNA合成减少；然而，低浓度（<9微克/孔）的LPS在静止和非静止细胞中显示出DNA合成的最小增强（40%至60%）。与生长因子刺激的对照相比，与促有丝分裂剂和LPS（9微克/孔）共同孵育的HGF表现出对生长因子诱导的3H-Tdr摄取的抑制。相反，添加低浓度（0.09微克/孔）的LPS会使3H-Tdr摄取略有升高。在所有测试的生长因子中都观察到了这些趋势。一般来说，与静止的HGF相比，非静止细胞对生长因子以及LPS/生长因子组合的反应更敏感。通过在生长因子孵育前用LPS预处理细胞，以及随后向生长因子预处理的细胞中添加LPS，进一步测试了HGF中LPS改变生长因子反应性的能力。观察到与上述类似的模式，除了与IL-1β刺激的对照相比，IL-1β预处理的静止和非静止HGF随后添加LPS显示出增殖明显升高。这些发现表明，LPS可能潜在地调节牙周病变中经历炎症或生长因子诱导的修复过程的结缔组织的增殖率。
