Phagocytosis is differentially regulated by LPS in M1- and M2-like macrophages via PGE2 formation and EP4 signaling.

According to a preprint abstract, phagocytosis is an important process in the human innate immune response. Macrophages, a type of immune cell, play a crucial role in phagocytosis by engulfing and neutralizing pathogens and cell debris. They also release cytokines and lipid mediators to modulate inflammation. The link between oxylipins (lipid mediators) and phagocytosis in different macrophage phenotypes is not well understood. In this study, researchers investigated the relationship between phagocytosis and the arachidonic acid (ARA) cascade in primary human macrophages. They found that M1-like macrophages, which are inflammatory, had higher levels of cyclooxygenase (COX)-2 and its products after stimulation with LPS (lipopolysaccharide) compared to M2-like macrophages, which are anti-inflammatory. LPS increased phagocytosis in M2-like macrophages but not in M1-like macrophages. The researchers also discovered that the COX product PGE2 modulates the effects of LPS on phagocytosis through the EP4 receptor. This finding suggests that blocking COX, such as with NSAIDs, could increase phagocytosis in inflammatory M1-like macrophages and potentially shift their phenotype towards a more pro-resolving state. However, it is important to note that this preprint has not yet [Extracted from the article]