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Recent studies have demonstrated that a variety of chemokine receptors are expressed in mast cells. We investigated the changes in mRNA expression of CXCRs in murine IL-3-dependent bone marrow-derived mast cells (BMMCs) to clarify how the CXCR expression is regulated in mast cells.Expression of CXCR mRNA was measured by RNase protection assay. Functional expression of CXCRs was confirmed by monitoring intracellular Ca(2+) mobilization.CXCR4 mRNA expression was transiently induced in BMMCs in serum-dependent fashion and was completely suppressed upon IgE-mediated antigen stimulation. In contrast, CXCR5 mRNA expression was induced upon IgE-mediated antigen stimulation. Changes in the intracellular Ca(2+) mobilization induced by CXCL12 strongly indicated the functional expression of CXCR4. The decrease in CXCR4 and the increase in CXCR5 mRNA expression was also observed in BMMCs stimulated with thapsigargin, a phorbol ester, and stem cell factor.The mRNA expression of CXCR4 is differentially regulated in BMMCs upon various stimuli including IgE-mediated antigen stimulation.

It remains to be fully clarified how adhesion of mast cells is regulated in vivo. We previously reported that PGE2-receptor EP4 stimulated the adhesion of mouse mastocytoma P-815 cells to plate-bound fibronectin. Our purpose in this study is to evaluate the adhesion using a system, which can mimic the in vivo adhesion.P-815 cells were transplanted in an air pouch produced in the transplantable mice, CDF1. The number of cells that adhere to the subcutaneous tissues overlaying the inside cavity surface was determined.The number of adhered cells was decreased in mice administered with ibuprofen or an EP4 antagonist, ONO AE3-208. A local administration of PGE(2) or a phorbol ester, PMA, increased the number of adhered cells, which was also suppressed in the mice treated with ONO AE3-208.Our results suggest that PGE(2)-mediated adhesion of P-815 cells in the subcutaneous tissues of the air pouch is mediated by the EP4 subtype.