Neutrophils alter epithelial response to Porphyromonas gingivalis in a gingival crevice model.
Neutrophils alter epithelial response to Porphyromonas gingivalis in a gingival crevice model.
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DOI：
10.1111/omi.12008
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发表时间：
2013-04
影响因子：
3.7
通讯作者：
Scott DA
中科院分区：
文献类型：
--
作者：
Bondy-Carey JL;Galicia J;Bagaitkar J;Potempa JS;Potempa B;Kinane DF;Veillard F;Scott DA
建立牙龈裂隙模型（上皮细胞-牙龈卟啉单胞菌-中性粒细胞），并用于分析牙龈蛋白酶、基质金属蛋白酶、MMP介质（NGAL和TIMP-1）和细胞因子网络。吸烟是牙周炎的主要环境危险因素。因此，在同一模型中也监测了香烟烟雾提取物（CSE）的影响。单独的牙龈卟啉单胞菌从上皮细胞诱导低水平的IL-1β和IL-8，但在加入中性粒细胞时产生高水平的两种细胞因子。CSE暴露（100和1000 ng/ml尼古丁当量）显著损害牙龈卟啉单胞菌诱导的细胞因子分泌（均p < 0.05）。牙龈卟啉单胞菌诱导显著的NGAL分泌（p < 0.05），其不受CSE的影响。CSE对牙龈卟啉酶产生的影响具有菌株特异性。纯化的牙龈卟啉菌蛋白酶有效且快速地降解TIMP-1和MMP-9。大量NGAL的诱导、TIMP-1的降解和牙龈菌蛋白酶活性的增加将各自预期延长胶原降解并促进疾病进展。然而，牙龈卟啉菌蛋白酶也降解MMP-9。因此，牙龈卟啉单胞菌对牙龈裂隙模型的蛋白水解平衡产生复杂的影响。CSE暴露降低了促炎细胞因子负荷，这可能会促进牙龈卟啉单胞菌的存活。除了提供牙周病进展机制的新发现外，这些结果与公认的吸烟者炎症减少/疾病增加的临床教条一致。因此，这个简单的龈沟模型建立作为一个合适的车辆的机制，有助于牙周炎的易感性阐明。
A gingival crevice model (epithelial cell- Porphyromonas gingivalis – neutrophil) was established and used to profile gingipain, matrix metalloproteinase, MMP mediators (NGAL and TIMP-1) and cytokine networks. Smoking is the primary environmental risk factor for periodontitis. Therefore, the influence of cigarette smoke extract (CSE) was also monitored in the same model. P. gingivalis alone induced low levels of IL-1β and IL-8 from epithelial cells, but high levels of both cytokines were produced on the addition of neutrophils. CSE-exposure (100 and 1000 ng/ml nicotine equivalency) significantly compromised P. gingivalis-induced cytokine secretion (both p < 0.05). P. gingivalis induced impressive secretion of NGAL (p < 0.05) which was not influenced by CSE. The influence of CSE on gingipains production was strain-specific. Purified gingipains effectively and rapidly degraded both TIMP-1 and MMP-9. Induction of large amounts of NGAL, degradation of TIMP-1, and increased gingipain activity would each be expected to prolong collagen degradation and promote disease progression. However, gingipains also degrade MMP-9. Thus, P. gingivalis exerts a complex influence on the proteolytic balance of a gingival crevice model. CSE-exposure reduces the pro-inflammatory cytokine burden, which may be expected to promote P. gingivalis survival. In addition to novel findings that provide mechanistic insight into periodontal disease progression, these results are in keeping with the recognized clinical dogma of decreased inflammation / increased disease in smokers. Thus, this straightforward gingival crevice model is established as a suitable vehicle for the elucidation of mechanisms that contribute to susceptibility to periodontitis.
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影响因子：
3.7
作者：
Dickinson BC;Moffatt CE;Hagerty D;Whitmore SE;Brown TA;Graves DT;Lamont RJ
通讯作者：
Lamont RJ
影响因子：
3.7
作者：
Bagaitkar J;Daep CA;Patel CK;Renaud DE;Demuth DR;Scott DA
通讯作者：
Scott DA
DOI：
10.1016/j.bbadis.2006.05.014
发表时间：
2006-08-01
影响因子：
6.2
作者：
Liu, K. -Z.;Hynes, A.;Scott, D. A.
通讯作者：
Scott, D. A.
影响因子：
4.2
作者：
Guggenheim, Bernhard;Gmuer, Rudolf;Kinane, Denis F.
通讯作者：
Kinane, Denis F.
影响因子：
16
作者：
Goetz, DH;Holmes, MA;Strong, RK
通讯作者：
Strong, RK