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Immune network analysis of cerebrospinal fluid in myalgic encephalomyelitis/chronic fatigue syndrome with atypical

M Hornig1,2, C G Gottschalk3, M L Eddy1

  • 1Center for Infection and Immunity, Columbia University Mailman School of Public Health, New York, NY, USA.

Translational Psychiatry
|April 5, 2017
PubMed

Insights

Atypical Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) cases show distinct immune signatures in cerebrospinal fluid, differing from classical ME/CFS presentations. Lower levels of specific inflammatory mediators are associated with atypical ME/CFS phenotypes.

Area of Science:

  • Neuroimmunology
  • Infectious Disease Immunology

Background:

  • Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a complex, debilitating illness characterized by fatigue, cognitive dysfunction, and sensory issues.
  • While classical ME/CFS often follows an infection, atypical presentations with unique comorbidities complicate diagnosis and understanding.
  • Investigating central nervous system immune markers is crucial for differentiating ME/CFS subtypes.

Purpose of the Study:

  • To compare cerebrospinal fluid (CSF) cytokine profiles between classical and atypical ME/CFS cases.
  • To identify immune molecules associated with the atypical ME/CFS phenotype.
  • To explore differences in immune network interactions within the CSF of ME/CFS subtypes.

Main Methods:

  • Analysis of CSF from 32 classical and 27 atypical ME/CFS patients using a 51-plex cytokine assay.
  • Logistic regression modeling with feature selection to identify predictor variables.
  • Network analysis to examine inter-cytokine relationships.

Main Results:

  • Significant differences in CSF cytokine profiles were observed between classical and atypical ME/CFS groups.
  • Lower CSF levels of interleukin-17A and CXCL9 were strongly associated with the atypical ME/CFS phenotype.
  • Atypical ME/CFS patients lacked inverse inter-cytokine relationships and had sparser positive correlations compared to classical ME/CFS patients.

Conclusions:

  • Immune signatures in the central nervous system may differ between classical and atypical ME/CFS presentations.
  • Disturbances in interleukin-1 signaling and autoimmunity-like immune activation patterns were suggested in classical ME/CFS.
  • These findings highlight distinct neuroinflammatory pathways in ME/CFS subtypes, aiding differential diagnosis.

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