1 National Central University, Taoyuan City, Taiwan.
2 Landseed Hospital, Taoyuan City, Taiwan.
Innate Immun. 2018 Nov;24(8):501-512. doi: 10.1177/1753425918809155.
Macrophage migration is an essential step in host defense against infection and wound healing. Elevation of cAMP by inhibiting phosphodiesterase 4 (PDE4), enzymes that specifically degrade cAMP, is known to suppress various inflammatory responses in activated macrophages, but the role of PDE4 in macrophage migration is poorly understood. Here we show that the migration of Raw 264.7 macrophages stimulated with LPS was markedly and dose-dependently induced by the PDE4 inhibitor rolipram as assessed by scratch wound healing assay. Additionally, this response required the involvement of serum in the culture medium as serum starvation abrogated the effect. Further analysis revealed that rolipram and serum exhibited synergistic effect on the migration, and the influence of serum was independent of PDE4 mRNA expression in LPS-stimulated macrophages. Moreover, the enhanced migration by rolipram was mediated by activating cAMP/exchange proteins directly activated by cAMP (Epac) signaling, presumably via interaction with LPS/TLR4 signaling with the participation of unknown serum components. These results suggest that PDE4 inhibitors, together with serum components, may serve as positive regulators of macrophage recruitment for more efficient pathogen clearance and wound repair.
巨噬细胞迁移是宿主抗感染和伤口愈合的重要步骤。通过抑制磷酸二酯酶 4(PDE4)升高 cAMP,该酶特异性降解 cAMP,已知可抑制激活的巨噬细胞中的各种炎症反应,但 PDE4 在巨噬细胞迁移中的作用知之甚少。在这里,我们发现 LPS 刺激的 Raw 264.7 巨噬细胞的迁移通过划痕愈合试验明显且呈剂量依赖性地被 PDE4 抑制剂罗利普兰诱导。此外,该反应需要培养基中血清的参与,因为血清饥饿会消除这种作用。进一步分析表明,罗利普兰和血清对迁移具有协同作用,并且血清的影响独立于 LPS 刺激的巨噬细胞中 PDE4 mRNA 的表达。此外,罗利普兰增强的迁移是通过激活 cAMP/直接被 cAMP 激活的交换蛋白(Epac)信号转导介导的,推测是通过与 LPS/TLR4 信号转导相互作用,同时涉及未知的血清成分。这些结果表明,PDE4 抑制剂与血清成分一起可能作为巨噬细胞募集的正调节剂,以更有效地清除病原体和修复伤口。