The high-affinity IgE receptor FcεRI 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 FcεRI expression in human basophilic KU812 cells was studied. The PPARα ligand, leukotriene B4, did not affect the cell surface expression of FcεRI. However, prostaglandin (PG) A1 and 15-deoxy-Δ12,14 PGJ2 (15d-PGJ2), which are PPARβ and γ ligands, respectively, were both able to decrease FcεRI expression. Treatment with PGA1 or 15d-PGJ2 separately also reduced histamine release from KU812 cells in response to cross-linkage of FcεRI. In addition, RT-PCR analysis showed that KU812 cells expressed the mRNA for PPARα, β, and γ, indicating that PPARβ or γ may negatively regulate the cell activation via FcεRI. Cells treated with 15d-PGJ2 expressed lower levels of FcεRIα and γ mRNA, and PGA1 treatment decreased the level of FcεRIγ mRNA. These results suggest that the suppression of FcεRI expression by PPARs may be due to the down-regulation of FcεRIα or γ mRNA.
|Number of pages||9|
|Journal||Biochemical and Biophysical Research Communications|
|Publication status||Published - Nov 6 2002|
All Science Journal Classification (ASJC) codes
- Molecular Biology