BRS6 → BRS3 — Stress Signalling Interactions with Inflammatory Load
Neuroendocrine and autonomic stress signalling from BRS6 can raise inflammatory and redox load in BRS3.
Dependency
HPA-axis mediators, autonomic imbalance and metabolic stress can activate immune signalling. BRS3 then determines cytokine tone, oxidative burden and resolution. This is a stress-to-inflammation bridge, not an immune-system substitute for BRS6.
Principal Routes
| Route | Contribution to BRS3 | Relationship |
|---|---|---|
| HPA / glucocorticoid signalling | Can increase inflammatory and oxidative mediators | Direct |
| Autonomic imbalance | Can favour sympathetic-linked inflammatory tone | Conditional |
Network Interpretation
Gut-origin immune signals belong on BRS5 → BRS3. Transmitter consequences of inflammatory load belong on BRS3 → BRS1 as BRS6 → BRS3 → BRS1.
Boundary and Evidence Status
Stress–inflammation coupling is supported by systems reviews. A single omega-3 trial in stressed adults does not validate the full dependency or an ADHD treatment. Cytokine biology remains owned by BRS3-FM3-PM7.
Supporting Evidence
- Slavich and Irwin, 2014 — Reviews social and psychological stress as inflammatory signals reshaping neuroimmune biology.
- McEwen, 2006 — Reviews bidirectional interactions between stress mediators and immune-inflammatory processes.
- Kiecolt-Glaser et al., 2011 — Trial in stressed adults: omega-3 reduced selected inflammatory cytokines alongside anxiety symptoms. This is a translational example, not proof of the BRS6 → BRS3 cascade.