Dorta-Aguilar 2023 — Gut permeability and bacterial translocation in FM and ME/CFS

One-paragraph summary

Multicenter pilot ELISA study comparing plasma levels of intestinal-barrier and bacterial-translocation markers in fibromyalgia and ME/CFS patients vs. matched healthy controls. FM patients showed significantly elevated plasma anti-β-LGB antibodies, zonulin-1 (ZO-1), LPS, and sCD14 vs. controls. This is the direct FM-patient empirical anchor for the intestinal_permeability mechanism that the project previously had only as Kishore 2026 review-tier evidence. Elevation of all four markers (barrier compromise + bacterial translocation + systemic immune activation) is internally consistent: the gut barrier is compromised, microbial products translocate into circulation, and the systemic immune system reacts. Anti-β-LGB (anti-bovine-β-lactoglobulin) antibodies suggest dietary protein leakage in particular, providing a candidate immune-trigger link to the autoantibody axis.

Claims as triples

• intestinal_permeability — present_in → fm_autoimmune [evidence: zonulin-1 elevated; confidence: emerging]
• serum_zonulin_level — predicts → intestinal_permeability [evidence: ELISA elevation in FM vs HC; confidence: emerging]
• serum_LPS_level — predicts → intestinal_permeability [evidence: ELISA elevation in FM vs HC; confidence: emerging]
• LPS — modulates → neuroinflammation_glial [bridging from broader literature; confidence: bridging]
• sCD14 — correlates_with → intestinal_permeability [evidence: co-elevation with LPS; confidence: emerging]

Methods note

Multicenter pilot study. ELISA quantification of plasma anti-β-LGB IgG, zonulin-1 (ZO-1), LPS, sCD14, and IL-1β in FM patients, ME/CFS patients, and healthy controls. Sample size and exact statistical results require full-text retrieval to specify.

Limitations

• Cross-sectional. Doesn't establish that intestinal permeability precedes FM symptoms.
• Did not stratify by anti-SGC IgG status — cannot directly link gut permeability to the autoimmune subtype.
• Pilot sample size; replication needed at larger scale.
• Single-timepoint measurement; doesn't capture temporal dynamics.
• Anti-β-LGB elevation is suggestive of dietary-protein translocation but the direct causal arrow to FM symptoms is unproven.

Open questions raised

• Do anti-SGC-IgG-positive FM patients have higher zonulin/LPS than IgG-negative FM patients? (Direct test of the H1 chain in stratified cohort.)
• Does an oral mannitol/lactulose ratio test (gold-standard intestinal permeability measure) confirm the ELISA-based zonulin finding?
• Does the bacterial-translocation signature predict which FM patients respond to FMT in subsequent trials?

Triangulation notes

• Strongly upgrades H1's upstream link from review-tier (Kishore 2026) to primary-data (this paper). The mechanism map's H1 chain now has primary-data backing at every link except the BA→IgG arrow that BASIS-FM tests.
• Connects to bridge B2 (Microbiome ↔ FM via gut-brain axis): gives a measurable mid-chain biomarker (zonulin) that a microbiome-modulation trial could use as an engagement marker.
• The ME/CFS co-finding strengthens bridge B4 (ME/CFS shared neuroimmune mechanism) at the gut-immune level.

Bridges

• B2 reinforced: zonulin/LPS as the clinically usable engagement-marker chain between microbiome dysbiosis and downstream immune activation.
• B4 reinforced: same mechanism in FM and ME/CFS suggests shared etiology at the gut-immune layer.