Department of Microbiology and Immunology, School of Medicine, Kangwon National University, Chuncheon 200-701, Korea.
Immune Netw. 2011 Dec;11(6):364-7. doi: 10.4110/in.2011.11.6.364. Epub 2011 Dec 31.
Prostaglandins (PGs) play pathogenic and protective roles in inflammatory diseases. The novel concept of PGs as immune modulators is being documented by several investigators. By establishing an in vitro experimental model containing human follicular dendritic cell-like cells, HK cells, we reported that HK cells produce prostaglandin E(2) (PGE(2)) and prostaglandin I(2) (PGI(2)) and that these PGs regulate biological functions of T and B cells.
To investigate the respective contribution of cyclooxygenase-1 (COX-1) and COX-2 to PGE(2) and PGI(2) production in HK cells, we performed siRNA technology to knock down COX enzymes and examined the effect on PG production.
Both PGE(2) and PGI(2) productions were almost completely inhibited by the depletion of COX-2. In contrast, COX-1 knockdown did not significantly affect PG production induced by lipopolysaccharide (LPS).
The current results suggest that mPGES-1 and PGIS are coupled with COX-2 but not with COX-1 in human follicular dendritic cell (FDC) and may help understand the potential effects of selective COX inhibitors on the humoral immunity.
前列腺素（PGs）在炎症性疾病中具有致病和保护作用。几位研究人员记录了 PG 作为免疫调节剂的新概念。通过建立包含人滤泡树突状细胞样细胞 HK 细胞的体外实验模型，我们报道 HK 细胞产生前列腺素 E2（PGE2）和前列腺素 I2（PGI2），这些 PG 调节 T 和 B 细胞的生物学功能。
为了研究环氧合酶-1（COX-1）和 COX-2 对 HK 细胞中 PGE2 和 PGI2 产生的各自贡献，我们使用 siRNA 技术敲低 COX 酶并检查其对 PG 产生的影响。
COX-2 的耗竭几乎完全抑制了 PGE2 和 PGI2 的产生。相比之下，COX-1 敲低对脂多糖（LPS）诱导的 PG 产生没有显著影响。
目前的结果表明，mPGES-1 和 PGIS 与 COX-2 而不是 COX-1 偶联在人滤泡树突状细胞（FDC）中，并可能有助于理解选择性 COX 抑制剂对体液免疫的潜在影响。
