Condition Focus: Lung Fibrosis — Dual Anti-Inflammatory and Anti-Fibrotic Effects at 660nm
While the lung may seem far removed from gout, this study from Brochetti and colleagues demonstrates a principle that applies directly to chronic tophaceous joint disease: PBM at 660 nm can reduce both active inflammation and established fibrosis simultaneously, using a single intervention.
In a bleomycin-induced lung fibrosis model, 660 nm PBM at 5 J/cm² reduced inflammatory cell infiltration, suppressed IL-6 and CXCL1/KC (a neutrophil-attracting chemokine), decreased collagen production, and reduced interstitial thickening (the tissue-level manifestation of fibrosis). These effects were achieved with no reported side effects — the authors noted PBM as an “economical therapy” with dual mechanism.
The dual mechanism is the key insight for gout. In chronic tophaceous gout, patients have both active inflammation (ongoing flares, subclinical inflammation between flares) and established fibrosis (the collagenous shell around tophi, joint capsule thickening, tendon scarring). Most treatments address one or the other: NSAIDs and colchicine target inflammation; there is currently no pharmacological treatment specifically targeting gouty fibrosis. PBM’s ability to address both pathways simultaneously fills this therapeutic gap.
The 660 nm wavelength and 5 J/cm² energy density are close to the G.O.A.T.’s specifications (660 nm, 4 J/cm²), making this study directly relevant to the device’s expected tissue-level effects.
G.O.A.T. for Gout Alignment:
The G.O.A.T.’s 660 nm wavelength at 4 J/cm² closely matches the 660 nm at 5 J/cm² used in this study. The dual anti-inflammatory + anti-fibrotic effect demonstrated here supports the G.O.A.T.’s positioning for chronic gout management where both active disease and chronic tissue changes coexist.
Link to original research here
Editor’s note: The simultaneous anti-inflammatory and anti-fibrotic effects at 660 nm demonstrated here complement the transcriptomic anti-fibrotic evidence in Jagdeo et al 2021. The TGF-β/Smad pathway context is provided by PBM in Keloid Management 2025. The IL-6 suppression connects to the four-cytokine panel in Tomazoni et al 2017. The myofibroblast transition that drives the fibrosis reduced here is reviewed in PBM and Fibrosis Prevention 2025.
Related Articles
- Transcriptome Analysis: Red Light Activates Anti-Fibrotic Genes – Jagdeo et al 2021
- PBM in Keloid Management: Anti-Fibrotic Mechanisms – 2025
- Effects of PBM on Inflammatory Response in Experimental OA – Tomazoni et al 2017
- PBM as Prevention/Treatment for Fibrosis – 2025
- PBM, Cells of Connective Tissue and Repair – Houreld et al 2022
Key Takeaways
- 660 nm PBM reduces both inflammation AND fibrosis simultaneously — dual mechanism
- IL-6↓, CXCL1/KC↓, inflammatory cells↓, collagen↓, interstitial thickening↓
- No side effects — “economical therapy” with dual anti-inflammatory + anti-fibrotic action
- 5 J/cm² at 660 nm — close to G.O.A.T.’s 4 J/cm² at 660 nm specifications
Study Overview
| Study Type: | Controlled animal study (preclinical) |
| Wavelength(s): | 660 nm (±20 nm) |
| Treatment Protocol: | 5 J/cm² (15 J total); bleomycin-induced lung fibrosis |
| Sample Size: | Multiple mouse groups |
| Primary Outcome: | Inflammatory cells↓, IL-6↓, collagen↓, interstitial thickening↓ |
Full Citation
Brochetti RA, et al. (2017). Photobiomodulation therapy improves both inflammatory and fibrotic parameters in experimental model of lung fibrosis in mice. Lasers in Medical Science, 32(8), 1825–1834. View Publication
