BRS5 → BRS3 — Gut–Immune Drivers of Inflammatory Tone
Gut barrier and microbial immune signalling can change inflammatory and redox tone in BRS3.
Dependency
BRS5 can present microbial products and barrier leakage to host immune sensing. That input may raise cytokine and oxidative load owned by BRS3. Gut tryptophan metabolism can also feed kynurenine-related chemistry that later reaches BRS1 as a mediated path.
Principal Routes
| Route | Contribution to BRS3 | Relationship |
|---|---|---|
| Barrier/microbial immune sensing | Can increase systemic inflammatory signalling | Conditional |
| Gut tryptophan / microbial metabolite traffic | Can alter precursor and neuroimmune metabolite supply | Conditional; downstream BRS1 effects are mediated |
Network Interpretation
This page is about inflammatory load, not neurotransmitter synthesis. Stress-driven inflammation remains BRS6 → BRS3 and should not be counted as a BRS5 product.
Boundary and Evidence Status
Barrier-to-inflammation biology is plausible, but the currently attached reviews do not demonstrate a quantitative gut-barrier lesion driving BRS3 in humans. O'Mahony et al. primarily review serotonin and tryptophan along the microbiome–gut–brain axis. Slavich and Irwin review stress-to-inflammation, which is a BRS6 route. The named dependency is retained as a framework interpretation pending stronger gut-immune evidence.
Supporting Evidence
- O'Mahony et al., 2015 — Reviews microbiota, tryptophan metabolism and serotonin along the gut–brain axis; it is not a barrier-integrity trial.
- Slavich and Irwin, 2014 — Reviews stress as an inflammatory signal; assigned here only as a caution that inflammatory load may originate in BRS6 rather than BRS5.