Increase of CCL20 expression by human gingival fibroblasts upon stimulation with cytokines and bacterial endotoxin
Increase of CCL20 expression by human gingival fibroblasts upon stimulation with cytokines and bacterial endotoxin
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DOI：
10.1111/j.1365-2249.2005.02912.x
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发表时间：
2005-11-01
影响因子：
4.6
通讯作者：
Matsuo, T
中科院分区：
文献类型：
--
作者：
Hosokawa, Y;Hosokawa, I;Matsuo, T
最近的研究表明，牙周病组织中有CCL 20的表达，牙周病组织中有大量的CCR 6阳性T细胞浸润。然而，尚不确定哪些细胞可以诱导CCL 20的产生。在本研究中，我们研究了由人牙龈成纤维细胞（HGF）培养的CCL 20生产的特性。在这里，我们报告说，白细胞介素-1 β（IL-1 β），肿瘤坏死因子-α（TNF-α）和大肠杆菌脂多糖（LPS）可以显着诱导肝细胞生长因子的生产CCL 20。我们发现TNF-α和E. coli LPS可促进IL-1 β诱导的HGF产生CCL 20。相比之下，干扰素-γ（IFN-γ）显著减少由IL-1 β诱导的CCL 20产生。此外，我们还证实了核因子-κ B（NF-κ B）、p38丝裂原活化蛋白激酶（MAPK）和细胞外信号调节激酶（ERK）在介导IL-1 β和TNF-α诱导的CCL 20产生中起重要作用。另一方面，我们发现在大肠杆菌诱导的CCL 20产生中，不仅有NF-κ B、p38 MAPK和ERK参与，c-Jun氨基末端激酶（JNK）也参与其中。coli LPS。最后，我们发现HGF表达CCR 6、CCL 20受体，以及CCL 20通过HGF诱导血管内皮生长因子（VEGF）的表达。综上所述，这些发现表明HGF将是牙周组织中CCL 20的来源，并且牙周病组织中CCL 20的产生将受到促炎细胞因子和细菌LPS的控制。因此，HGF诱导的CCL 20可能参与了炎症细胞的浸润，促进牙周病的进展。
We have demonstrated recently that CCL20 was expressed in periodontal diseased tissues and abundant CCR6 positive T cells infiltrated in periodontally diseased tissue. However, it is uncertain which cells can elicit CCL20 production. In the present study, we examined the properties of CCL20 production by human gingival fibroblasts (HGF) culture. Here, we report that interleukin-1 beta (IL-1 beta), tumour necrosis factor-alpha (TNF-alpha) and Escherichia coli lipopolysaccharide (LPS) can significantly induce the production of CCL20 by HGF. We found that TNF-alpha and E. coli LPS enhanced the production of CCL20 by HGF treated with IL-1 beta. In contrast, interferon-gamma (IFN-gamma) dramatically diminished CCL20 production induced by IL-1 beta. Moreover, we demonstrated that nuclear factor-kappaB (NF-kappa B), p38 mitogen-activated protein kinase (MAPK) and extracellular signal-regulated kinases (ERK) play an important role in mediating the production of CCL20 induced by IL-1 beta and TNF-alpha. On the other hand, we found that not only NF-kappa B, p38 MAPK and ERK but also c-Jun NH2-terminal kinase (JNK) are involved in CCL20 production induced by E. coli LPS. Finally, we found that HGF express CCR6, CCL20 receptor, and CCL20 induced vascular endothelial growth factor (VEGF) by HGF. Taken together, these findings that HGF will be a source of CCL20 in periodontal tissue, and the CCL20 production will be controlled by proinflammatory cytokine and bacterial LPS in periodontally diseased tissue. Thus, CCL20 by HGF might be involved in inflammatory cells infiltration, and promote the progression of periodontal disease.