2020
DOI: 10.1021/acsbiomaterials.9b01180
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Prostaglandin E2 and Its Receptor EP2 Modulate Macrophage Activation and Fusion in Vitro

Abstract: The foreign body response (FBR) has impaired progress of new implantable medical devices through its hallmark of chronic inflammation and foreign body giant cell (FBGC) formation leading to fibrous encapsulation. Macrophages are known to drive the FBR, but efforts to control macrophage polarization remain challenging. The goal for this study was to investigate whether prostaglandin E2 (PGE2), and specifically its receptors EP2 and/or EP4, attenuate classically activated (i.e., inflammatory) macrophages and mac… Show more

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Cited by 24 publications
(14 citation statements)
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“…S8), indicating that the beneficial effects of PGE 2 and PGI 2 on repair may be specific for the alveolar epithelial cell. In addition, studies have shown PGE 2 to be anti-inflammatory by attenuating macrophages activation and proliferation ( 39 , 49 ), While beneficial, the anti-inflammatory activity of PGE 2 and PGI 2 analogs could also predispose to pulmonary infections, which is a risk that needs to be considered moving forward. Here, we identified the potential therapeutic effect of PGE 2 and PGI 2 analogs on defective alveolar progenitors in response to CS that appears to be primarily related to the disturbance of circadian clock signaling rather than its anti-inflammatory response.…”
Section: Discussionmentioning
confidence: 99%
“…S8), indicating that the beneficial effects of PGE 2 and PGI 2 on repair may be specific for the alveolar epithelial cell. In addition, studies have shown PGE 2 to be anti-inflammatory by attenuating macrophages activation and proliferation ( 39 , 49 ), While beneficial, the anti-inflammatory activity of PGE 2 and PGI 2 analogs could also predispose to pulmonary infections, which is a risk that needs to be considered moving forward. Here, we identified the potential therapeutic effect of PGE 2 and PGI 2 analogs on defective alveolar progenitors in response to CS that appears to be primarily related to the disturbance of circadian clock signaling rather than its anti-inflammatory response.…”
Section: Discussionmentioning
confidence: 99%
“…Whereas the simultaneous presence of PGE 2 with palmitate ( Figure 3 ) or TNFα [ 28 ] enhanced IL-8 formation, the incubation of human alveolar macrophages with PGE 2 prior to subsequent stimulation with LPS inhibited the LPS-induced IL-8 formation in one study [ 29 ], whereas it was without effect in another [ 30 ]. Finally, PGE 2 may also inhibit TNFα formation in macrophages [ 31 , 32 ] and Kupffer cells [ 33 ], and thereby attenuate the inflammatory response. Currently, it is not clear which of these apparently opposing signaling pathways of PGE 2 is more relevant in vivo.…”
Section: Discussionmentioning
confidence: 99%
“…109 110 In macrophages, EP2 agonism suppresses phagocytosis, enhances IL-10 production, and decreases TNF-α production, and PGE2 upregulates COX-2 expression, in an EP2/4 dependent manner, creating an autocrine feedforward loop (figure 3). [111][112][113] Signaling through either EP2 or EP4 results in increased PD-1 expression in tumor-infiltrating CD8 + T cells of lung cancer patients (figure 3). 114 Because PGE2-mediated immunosuppression occurs via two receptors, targeting one may not fully prevent its impact.…”
Section: Pge2 Immunosuppressive Signaling Through Ep2 and Ep4mentioning
confidence: 99%