Condition Focus: Systemic Inflammation — NLRP3 Output Suppression via Dual-Wavelength PBM
This 2023 study from Shamloo and colleagues at Stanford represents the critical bridge between gout pathology and PBM therapy. Using an LPS-induced inflammation model in mice, the researchers demonstrated that dual-wavelength PBM (640 nm red + 880 nm near-infrared) suppressed the exact cytokines that the NLRP3 inflammasome produces in gout: IL-1β and IL-18. Simultaneously, PBM upregulated IL-10 — the anti-inflammatory cytokine that helps resolve inflammation.
The cytokine profile affected here — IL-1β down, IL-18 down, IL-10 up — is the mirror image of what happens during a gout flare (IL-1β up, IL-18 up, IL-10 insufficient). PBM effectively reverses the inflammatory cytokine signature.
The study also investigated a 40 Hz gamma frequency flicker modality and found it potentiated some anti-inflammatory effects, though the PBM-only arm showed robust results independently. The dual-wavelength approach — combining red and NIR simultaneously — is particularly relevant because it delivers both surface-tissue (red) and deep-tissue (NIR) effects in a single treatment session.
Importantly, this was measured at both systemic and central nervous system levels, demonstrating that PBM’s anti-inflammatory effects extend beyond the local treatment site. For gout patients, this suggests that even a locally applied device may help modulate the systemic inflammatory burden that accompanies chronic hyperuricaemia.
G.O.A.T. for Gout Alignment:
The dual-wavelength approach used here (640 nm + 880 nm) closely parallels the G.O.A.T.’s 660 nm + 850 nm configuration. The suppression of IL-1β and IL-18 — the two primary NLRP3 outputs in gout — represents direct evidence that dual-wavelength PBM opposes the gout inflammasome cascade. The G.O.A.T.’s design is built on this exact dual-wavelength principle.
Link to original research here
Editor’s note: This study provides the direct PBM-to-NLRP3 connection. The NLRP3 cascade that produces the IL-1β and IL-18 suppressed here is mapped in Kingsbury et al 2011. The NF-κB suppression mechanism upstream of cytokine production is detailed in Immunomodulatory Effects of PBM 2025. The macrophage phenotype shift that contributes to cytokine rebalancing is explored in M1→M2 Polarization Review 2025. For the TMJ inflammation model showing similar cytokine suppression with 808 nm, see TMJ Inflammation 2020.
Related Articles
- The Role of the NLRP3 Inflammasome in Gout – Kingsbury et al 2011
- Immunomodulatory Effects of PBM: Comprehensive Review – 2025
- PBM and Macrophage Polarization: M1→M2 Shift Review – 2025
- PBM Inhibits TMJ Inflammation and Reduces Edema – 2020
- MSU Crystals Activate the NALP3 Inflammasome – Martinon et al 2006
Key Takeaways
- Dual-wavelength PBM (640nm + 880nm) suppresses IL-1β and IL-18 — the exact NLRP3 outputs in gout
- IL-10 upregulated — reversing the inflammatory cytokine balance seen in gout flares
- Systemic and CNS anti-inflammatory effects demonstrated — not just local
- Dual-wavelength approach directly parallels the G.O.A.T.’s 660nm + 850nm design
Study Overview
| Study Type: | Controlled animal study (preclinical) |
| Wavelength(s): | 640 nm + 880 nm dual-wavelength; ± 40 Hz gamma flicker |
| Treatment Protocol: | PBM treatment following LPS-induced systemic inflammation |
| Sample Size: | Mouse model, multiple treatment groups |
| Primary Outcome: | IL-1β↓, IL-18↓, IL-10↑ in brain and peripheral tissue |
Full Citation
Shamloo S, Defensor E, Ciari P, et al. (2023). The anti-inflammatory effects of photobiomodulation are mediated by cytokines: evidence from a mouse model of inflammation. Frontiers in Neuroscience, 17, 1150156. View Publication
