From acute inflammation to chronic disease

Acute infection / other trigger
↓
Immune activation
↓
↑ PGE2
↓
EP-receptor adaptation + altered endocrine/immune signaling
↓
Persistent PGE2 activity
↓
Homeostatic and immune dysregulation
↓
Chronic post-infectious symptoms

This framework proposes that PGE2 may act as a mechanistic bridge between the initial trigger and the persistence of disease, rather than being merely a downstream marker of inflammation.

It may help connect apparently different mechanisms reported in Long COVID and related syndromes, including autoimmunity, GPCR autoantibodies, autonomic dysfunction, mitochondrial dysfunction, endothelial dysfunction and persistent inflammation.

one upstream mechanism could manifest through many apparently separate downstream mechanisms.