Prostaglandin E2Does Not Modulate CCR7 Expression and Functionality after Differentiation of Blood Monocytes into Macrophages

Previously, we demonstrated that prostaglandin E 2 (PGE 2 ) induces C-C chemokine receptor type 7 (CCR7) expression on human monocytes, which stimulates their subsequent migration in response to the CCR7 natural ligands CCL19 and CCL21. In this study, we determined whether PGE 2 affects CCR7 expression on macrophages. Flow cytometric analysis and chemotaxis assays were performed on Mono Mac-1-derived macrophage (MDMM-1) as well as unpolarized monocyte-derived macrophages (MDMs) to determine the CCR7 expression and functionality in the presence of PGE 2 . Data revealed that a MDMM-1 exhibited markedly downregulated CCR7 expression and functionality that were partially restored by treatment with PGE 2 . In MDMs, we observed a drastic downregulation of CCR7 expression and functionality that were unaffected following PGE 2 treatment. Our data indicate that monocyte differentiation induces the loss of CCR7 expression and that PGE 2 is unable to modulate CCR7 expression and functionality as shown previously in monocytes.