Widespread Myalgia and Chronic Fatigue: Phagocytes from Macrophagic Myofasciitis Patients Exposed to Aluminum Oxyhydroxide-Adjuvanted Vaccine Exhibit Specific Inflammatory, Autophagic, and Mitochondrial Responses.

Observed Findings

• MMF phagocytes uniquely expressed Rubicon and Nox2, molecular markers of the LAP autophagic pathway, distinguishing them from control cells
• MMF cells produced elevated levels of pain-inducing CXC chemokines and reduced TNF-α compared to controls after aluminum adjuvant exposure
• MMF phagocytes showed exaggerated metabolic activation in response to aluminum-adjuvanted vaccine but with markedly limited spare respiratory capacity
• MMF cells exhibited elevated proton leak in mitochondria, indicating energy production inefficiency
• MMF and control cells similarly internalized aluminum adjuvants, but cellular responses diverged significantly afterward

Inferred Conclusions

• MMF phagocytes employ a non-canonical autophagy pathway (LAP) to process persistent vaccine aluminum particles, which may perpetuate chronic immune signaling
• Dysregulated chemokine secretion in MMF cells provides a mechanistic explanation for the myalgia and exhaustion observed in ME/CFS-like symptomatology
• Mitochondrial dysfunction with limited energy reserve capacity suggests MMF patients have reduced physiological capacity to sustain normal activity levels
• Aluminum adjuvant persistence combined with altered cellular metabolism may create a chronic state of immune activation and energy depletion characteristic of ME/CFS

Remaining Questions