Abstract

Dendritic cells (DCs) are the most potent antigen-presenting cells, and are indispensable in the immune system. Prostaglandin E2 (PGE2) has been demonstrated to modulate the migration of DCs, but with inconsistent results. The present study, based on our previous research, used murine bone marrow-derived DCs to elucidate the potential regulatory mechanism of PGE2 on the migration of DCs. The results indicated that PGE2 served a dual role in regulating the migration of DCs in a dose-dependent manner. High concentrations of PGE2 inhibited cell migration, whereas low concentrations exhibited the opposite effect. Flow cytometry revealed that the expression of CC chemokine receptor type 7 on the DC surface was increased following treatment with low concentrations of PGE2 and slightly decreased by high concentrations of PGE2. The effect of PGE2 was indicated to be exerted via reorganizing the F-actin cytoskeleton using confocal micros-copy. Moreover, the regulatory effect of PGE2 on the migration of DCs was validated in vivo. Subsequent gene expression profile analyses using RNA-sequencing technology indicated that PGE2 induced alterations in the expression of multiple downstream genes and signaling pathway molecules associated with cell migration and the cytoskeleton. These findings may provide an improved understanding on the mechanism of DC migration under both pathological and physiological conditions. Moreover, the biological implications of these findings may provide a novel perspective of the immunological surveillance in the progression of different types of diseases.

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