Fujimura Yoshinori, Tachibana Hirofumi, Yamada Koji
Department of Bioscience and Biotechnology, Faculty of Agriculture, Division of Bioresources and Bioenvironmental Sciences, Kyushu University, 6-10-1 Hakozaki, Higashi-ku, Fukuoka 812-8581, Japan.
Biochem Biophys Res Commun. 2002 Sep 20;297(2):193-201. doi: 10.1016/s0006-291x(02)02139-3.
The high-affinity IgE receptor Fc epsilon RI is expressed on the cell surface of mast cells and basophils, and plays a central role in IgE-mediated inflammatory reactions. Recently, peroxisome proliferator-activated receptors (PPARs) have been implicated in the anti-inflammatory response. To investigate a possible role for PPAR in human basophils, the effect of PPAR ligands on Fc epsilon RI expression in human basophilic KU812 cells was studied. The PPARalpha ligand, leukotriene B(4), did not affect the cell surface expression of Fc epsilon RI. However, prostaglandin (PG) A(1) and 15-deoxy-Delta(12,14) PGJ(2) (15d-PGJ(2)), which are PPARbeta and gamma ligands, respectively, were both able to decrease Fc epsilon RI expression. Treatment with PGA(1) or 15d-PGJ(2) separately also reduced histamine release from KU812 cells in response to cross-linkage of Fc epsilon RI. In addition, RT-PCR analysis showed that KU812 cells expressed the mRNA for PPARalpha, beta, and gamma, indicating that PPARbeta or gamma may negatively regulate the cell activation via Fc epsilon RI. Cells treated with 15d-PGJ(2) expressed lower levels of Fc epsilon RI alpha and gamma mRNA, and PGA(1) treatment decreased the level of Fc epsilon RI gamma mRNA. These results suggest that the suppression of Fc epsilon RI expression by PPARs may be due to the down-regulation of Fc epsilon RI alpha or gamma mRNA.
高亲和力IgE受体FcεRI表达于肥大细胞和嗜碱性粒细胞的细胞表面，在IgE介导的炎症反应中起核心作用。最近，过氧化物酶体增殖物激活受体（PPARs）与抗炎反应有关。为了研究PPAR在人嗜碱性粒细胞中的可能作用，研究了PPAR配体对人嗜碱性KU812细胞中FcεRI表达的影响。PPARα配体白三烯B4不影响FcεRI的细胞表面表达。然而，分别作为PPARβ和γ配体的前列腺素（PG）A1和15-脱氧-Δ12,14-PGJ2（15d-PGJ2）均能降低FcεRI表达。单独用PGA1或15d-PGJ2处理也能减少KU812细胞因FcεRI交联而释放的组胺。此外，RT-PCR分析显示KU812细胞表达PPARα、β和γ的mRNA，表明PPARβ或γ可能通过FcεRI负向调节细胞活化。用15d-PGJ2处理的细胞表达较低水平的FcεRIα和γmRNA，而PGA1处理降低了FcεRIγmRNA的水平。这些结果表明，PPARs对FcεRI表达的抑制可能是由于FcεRIα或γmRNA的下调所致。
