This episode explains why some diseases never turn off.
Acute inflammation protects you. Chronic inflammation becomes the disease.
The difference is cytokine signaling.
Acute inflammation is chemistry. Chronic inflammation is immune programming.
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After the early inflammatory mediators fade, the immune system decides:
When cytokines remain active β inflammation sustains itself.
This is the basis of autoimmune disease.
| Cytokine | Major Role | Associated Diseases |
|---|---|---|
| TNF-Ξ± | Master inflammatory amplifier | RA, IBD, psoriasis |
| IL-1 | Fever and systemic inflammation | Autoinflammatory syndromes |
| IL-6 | Acute phase response | RA, systemic inflammatory disease |
| IL-5 | Eosinophils | Allergic asthma |
| IL-4 / IL-13 | IgE & allergy signaling | Atopic disease |
| IL-17 | Neutrophil activation | Psoriasis, spondyloarthritis |
These do not cause symptoms briefly β they reprogram tissue behavior.
NSAIDs block prostaglandins.
Autoimmune disease is driven by:
β Immune cell activation β Cytokine signaling β Gene transcription
So NSAIDs reduce pain⦠but disease continues progressing.
| Level | Drug Types | Effect |
|---|---|---|
| Symptom | NSAIDs, antihistamines | Feel better |
| Broad suppression | Corticosteroids | Disease quiets temporarily |
| Immune modification | DMARDs | Disease slows |
| Targeted control | Biologics & JAK inhibitors | Disease mechanism blocked |
The higher the level β the closer you are to the cause.
Biologics do not suppress inflammation generally.
They block specific signals:
This is why they can succeed where steroids fail long-term.
| Condition | Mechanism Level |
|---|---|
| Osteoarthritis | Local mediator inflammation |
| Rheumatoid arthritis | Cytokine immune disease |
| Asthma (allergic) | Eosinophilic cytokine disease |
| Psoriasis | T-cell cytokine disease |
| Sepsis | Systemic cytokine storm |
Treatment success depends on matching the level.
You are not treating inflammation.
You are choosing which conversation in the immune system to interrupt.