Table 1.
SPMs’ in vitro effects on human macrophages in inflammatory contexts.
Macrophages | SPMs | Effects | References |
---|---|---|---|
Human monocyte-derived macrophages (M1-like, M2-like) | LXA4 (250nM) | Protect macrophages from apoptosis | (150) |
LXA4 (0.1-10nM) | Increase phagocytosis of zymosan particles | (151) | |
Human monocytes | LXA4 (ATL-1) (1-100µM) | Inhibit monocytes’ apoptosis | (152) |
Primary human macrophages | LXA4 (ATL-1) (100µM) | Increase phagocytosis Decrease secretion of pro-inflammatory cytokines |
(153) |
Human monocyte-derived macrophages (M1-like) | RvD1 (0.1-1nM) | Increase phagocytosis of microbial particles and apoptotic PMN | (154) |
RvD1 (0.1-10nM) | Increase phagocytosis of zymosan particles | (151) | |
RvD1 (10nM) | Switch M1-like to M2-like macrophages | (155) | |
Human alveolar macrophages | RvD1 and RvD2 (100 nM) | Increase phagocytosis of microbial particles (E. coli) Decrease secretion of pro-inflammatory cytokines |
(156) |
Primary human macrophages | RvD1 (10nM) | Polarize resting primary macrophages and repolarize M1-like macrophages to a pro-resolving phenotype | (157) |
M1-like macrophages | RvD5 (10nM) | Increase phagocytosis of microbial particles | (67) |
Human monocyte-derived macrophages (M1-like) | RvE1 (10nM) | Increase phagocytosis of microbial particles | (158) |
Primary human macrophages | RvE1 (10nM) | Induce a pro-resolving phenotype | (159) |
Human monocyte derived macrophages (GM-CSF) | RvE2 (1-10nM) | Increase phagocytosis of zymosan particles | (160) |
Human macrophages (M2-like) | MaR1 (1 nM) | Increase efferocytosis of apoptotic PMN | (161) |
Human monocyte-derived macrophages (M1-like, M2-like) | MaR1 (10pM-10nM) | Increase phagocytosis (E. coli, zymosan) and efferocytosis of apoptotic PMN | (19) |
Human monocyte-derived macrophages (M1-like) | MaR1 (10 nM) | Switch M1-like to M2-like macrophages | (155) |
Human macrophages | PD-1 (22-F-PD1) (0.001-10nM) | Increase macrophages’ efferocytosis of apoptotic PMN | (162) |
Bold, SPM analogs or receptor agonists.