Fig 1.

Fig 2.

Fig 3.

Fig S1.

Fig S2.

Roles of PGE2 and NO in the inflammatory functions of M1, M2, and trained macrophages
| Feature | M1 macrophages (classically activated) | M2 macrophages (alternatively activated) | Trained macrophages (highPGE2/lowNO) |
|---|---|---|---|
| Activation stimuli | LPS, IFN-γ, TNF-α | IL-4, IL-13, IL-10, glucocorticoids | S. cerevisiae BG |
| COX-2 expression/PGE2 secretion | High/High | Low-moderate/low | High/high |
| Functional role of PGE2 | Pro-inflammatory; promotes IL-6, IL-1β | Anti-inflammatory; promotes tissue repair, fibrosis | Promotes neutrophil apoptosis and efferocytosis. Tissue repair. |
| iNOS | Strongly induced | Weak or absent | Weak or absent |
| NO production | High (major molecule for pathogen killing) | Low (minimal cytotoxic activity) | Low (minimal cytotoxic activity) |
| Functional role of NO | Microbicidal; contributes to oxidative stress | Suppresses inflammation; promotes healing indirectly (low NO maintains tissue integrity) | Suppresses inflammation; promotes healing indirectly (low NO maintains tissue integrity) |
| Beneficial functions | Early stages of infection/inflammation. Cooperation with neutrophils in pathogen killing | Resolution of inflammation. Efferocytosis of apoptotic neutrophils | Late stages of infection/inflammation. Recruitment of naïve macrophages. Resolution of chronic inflammation. Reduction of hyperinflammatory response |