Porphyromonas gingivalis and Escherichia coli lipopolysaccharide causes resistin release from neutrophils
Porphyromonas gingivalis and Escherichia coli lipopolysaccharide causes resistin release from neutrophils
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DOI：
10.1111/odi.12027
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发表时间：
2013-07-01
期刊：
影响因子：
3.8
通讯作者：
Saito, T.
中科院分区：
文献类型：
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作者：
Furugen, R.;Hayashida, H.;Saito, T.
注意事项：据报道，牙周炎与血清中的前列腺素水平升高有关。我们研究了中性粒细胞在牙龈卟啉单胞菌脂多糖（LPS）和大肠杆菌脂多糖（LPS）孵育下释放Ign是否存在差异，以及哪些细胞表面受体和细胞内激酶参与了这一过程。将coli-LPS加入到中性粒细胞中，收集来自培养的中性粒细胞的上清液，并通过ELISA测量β-内酰胺酶水平。用抗CD 14、CD 18、TLR 2、TLR 4单克隆抗体及PI 3 K和MAPK特异性抑制剂预处理中性粒细胞，检测其信号通路。coli-LPS对牙龈卟啉单胞菌的促分泌作用强于E.低浓度的coli-LPS。抵抗素释放减少预处理与单克隆抗体CD 14，CD 18，TLR 4，但不是TLR 2。此外，PI 3 K、JNK和p38 MAPK的抑制剂可降低中性粒细胞抵抗素的释放，而ERK 1/2则无此作用。coli-LPS。这是由CD 14，CD 18和TLR 4减少，并依赖于PI 3 K，JNK和p38 MAPK，但不依赖于ERK 1/2的细胞内途径的中性粒细胞。
OBJECTIVES: It was reported that periodontitis is associated with increased serum resistin levels. We examined whether there was a difference between the release of resistin from neutrophils incubated lipopolysaccharide (LPS) from Porphyromonas gingivalis and with LPS from Escherichia coli, and which cell-surface receptors and intracellular kinases were involved in this process.METHODS: Several concentrations of P. gingivalis-LPS and E. coli-LPS were added to neutrophils, supernatant from cultured neutrophils was collected, and resistin levels were measured by ELISA. To examine signaling pathways, neutrophils were pretreated with monoclonal antibodies against CD14, CD18, TLR2, and TLR4, and specific inhibitors of PI3K and MAPKs.RESULTS: Resistin release from neutrophils was induced both by P. gingivalis-LPS and E. coli-LPS, but resistin release by P. gingivalis-LPS was weaker than E. coli-LPS in low concentrations. Resistin release was decreased by pretreatment with monoclonal antibodies against CD14, CD18, and TLR4, but not by TLR2. Moreover, it was decreased by inhibitors of PI3K, JNK, and p38 MAPK, but not by ERK1/2.CONCLUSIONS: Resistin release from neutrophils was induced by both P. gingivalis-LPS and E. coli-LPS. This was decreased by CD14, CD18, and TLR4 and was dependent on PI3K, JNK, and p38 MAPK, but not on ERK1/2 in intracellular pathways of neutrophils.