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Monocytes play critical roles in human immunodeficiency virus type1 (HIV-1) pathogenesis. During HIV-1 infection, proinflammatory molecules such as prostaglandin E2 (PGE2) are observed at elevated levels in infected individuals. Mono-Mac-1 cells as well as freshly isolated monocytes were exposed to pseudotyped, R5 or dual tropic HIV-1 particles. CCR7 expression was determined by FACS analysis while chemotaxis assays were performed to show CCR7 functionality. We demonstrated that PGE2 enhanced CCR7 surface expression on monocytes. However, monocytes exposition to R5 or dual tropic HIV-1 particles did not highly modulate surface expression of CCR7. On the other hand, monocytes exposition to HIV-1 impaired the CCR7 dependent migratory capacity to CCL19. The addition of PGE2 to HIV-1-exposed monocytes restored the CCR7 dependent migration to levels similar to PGE2 treated unexposed monocytes. Monocytes acquired a functional responsiveness to CCL19 after exposure to PGE2 only when gp120 is expressed on viral particles. Finally, HIV-1-exposed monocytes that migrated in a Transwell system efficiently transmitted the infection to sensible cells. Collectively, we show that PGE2 is essential for the CCR7-dependent migration of monocytes exposed to HIV-1.

Exposure to HIV-1 Altered CCR7-Mediated Migration of Monocytes: Regulation by PGE2