Immunological role of prostaglandin E2 production in mouse auditory cells in response to LPS
Immunological role of prostaglandin E2 production in mouse auditory cells in response to LPS
复制标题
DOI：
10.1177/1753425913503578
复制
发表时间：
2014-08-01
期刊：
影响因子：
3.2
通讯作者：
Yokochi, Takashi
中科院分区：
文献类型：
--
作者：
Tanigawa, Tohru;Odkhuu, Erdenezaya;Yokochi, Takashi
本实验观察了脂多糖（LPS）对小鼠HEI-OC 1听觉细胞前列腺素E_2（PGE_2）产生的影响。HEI-OC 1听觉细胞组成性地产生少量的PGE 2。LPS通过增强环氧合酶2（COX 2）的表达来增加PGE 2的产生。LPS诱导的COX 2表达增强依赖于COX 2 mRNA表达的上调。LPS诱导TNF-α的产生，但不诱导IL-1的产生。抗TNF-α中和抗体显著抑制LPS诱导的PGE 2产生和COX 2 mRNA表达。LPS诱导的PGE 2的产生被一系列针对NF-B和MAPK的药理学信号传导抑制剂阻止。Pam 3CSK 4作为TLR 2配体，以及LPS作为TLR 4配体，增加PGE 2的产生。然而，作为TLR 3配体的poly I：C、作为TLR 7配体的咪喹莫特和作为TLR 9配体的CpG DNA并不增加其表达。LPS诱导的PGE 2的生产在听觉细胞的假定作用进行了讨论。
The effect of LPS on the production of prostaglandin E2 (PGE2) in mouse HEI-OC1 auditory cells was examined. HEI-OC1 auditory cells constitutively produce a small amount of PGE2. LPS augmented the PGE2 production via enhanced cyclooxygenase 2 (COX2) expression. LPS-induced augmentation of COX2 expression was dependent on up-regulation of COX2 mRNA expression. LPS induced the production of TNF-, but not IL-1 An anti-TNF- neutralizing Ab significantly inhibited PGE2 production and COX2 mRNA expression in response to LPS. LPS-induced PGE2 production was prevented by a series of pharmacological signaling inhibitors to NF-B and MAPKs. Pam3CSK4 as a TLR2 ligand, as well as LPS as a TLR4 ligand, augmented the PGE2 production. However, poly I:C as a TLR3 ligand, imiquimod as a TLR7 ligand and CpG DNA as a TLR9 ligand did not augment it. HEI-OC1 cells expressed TLR2, TLR4 and TLR9, but not TLR3 or TLR7. The putative role of LPS-induced PGE2 production in auditory cells is discussed.