TABLE 1.
Impact of CB receptor activation on macrophage polarization in different disease models
| Disease | Effect of CB1R signaling | Effect of CB2R signaling | Other treatments | Reference |
|---|---|---|---|---|
| Traumatic brain Injury (TBI) | Activation of CB2R using GP1a reduces neuroinflammation, promoting M2 polarization | (97) | ||
| Colorectal cancer | Activation of CB1R inhibits cancer cell proliferation, migration, and invasion and inhibits M2 polarization | (98) | ||
| Myofiber regeneration | Mice lacking CB2R (CB2R-KO) characterized by increased infiltration of M1 macrophages decrease in M2 macrophages | (99) | ||
| Cystic fibrosis (CF) | CB2R agonist downregulates M1 macrophage polarization and does not fully restore anti-inflammatory M2 macrophage polarization | (100) | ||
| Post-traumatic osteoarthritis | Activating CB2R shifts immune cell polarization away from pro-inflammatory states in mouse macrophages | (101) | ||
| Paraquat (PQ)-induced lung injury | WIN 55,212-2 increases the M2 macrophage numbers and reduces lung fibrosis | (102) | ||
| Liver fibrosis | CB1R blockade reduces M1-type bone marrow-derived monocytes/ macrophages | (103) | ||
| Alcoholic liver disease | CB2R activation using JWH-133 agonist reduces the expression of pro-inflammatory M1 genes in Kupffer cells without affecting the anti-inflammatory M2 profile | (104) | ||
| Spinal cord injury (SCI) | CB2R activation promotes M2 microglia differentiation, reduces pro-inflammatory cytokines | (105) | ||
| Acute liver failure | CB2R activation using JWH-133 agonist leads to macrophage polarization toward the M2 state while suppressing pro-inflammatory responses via miR-145 | (106) | ||
| LPS-induced inflammation | WIN 55,212–2 impairs pro-inflammatory M1 polarization in human macrophages and inhibits cytokine production and inflammasome activation | (107) |