Peripheral cytokines profile in Parkinson's disease

Brain Behav Immun. 2009 Jan;23(1):55-63. doi: 10.1016/j.bbi.2008.07.003. Epub 2008 Jul 17.


Higher levels of proinflammatory cytokines are found in Parkinson's disease (PD) patient's brains and inflammation is thought to be a major contributor to the neurodegeneration. During the inflammatory process, microglial release of proinflammatory cytokines act on the endothelium of blood-brain barrier (BBB) cells to stimulate upregulation of adhesion molecules. Consequently, this upregulation leads to the recruitment of passing T cells and monocytes, which express the counter receptors, that then go on to release more cytokines [Whitton, P.S., 2007. Inflammation as a causative factor in the aetiology of Parkinson's disease, Br. J. Pharmacol. 50, 963-976; Kortekaas, R., Leenders, K.L., Van Oostrom, J.C., Vaalburg, W., Bart, J., Willemsen, A.T., Hendrikse, N.H., 2005. Blood-brain barrier dysfunction in parkinsonian midbrain in vivo, Ann. Neurol. 57, 176-179]. In addition, a systemic inflammatory response results in the production of cytokines which circulate in the blood and communicate with neurons within the brain. Thus, a central inflammatory reaction interacts with peripheral blood mononuclear cells (PBMCs) modulating immune activity. The present study investigates levels of production and expression of cyto/chemokines by PBMCs in PD patients. Basal and LPS-induced levels of MCP-1, RANTES, MIP-1alpha, IL-8, IFNgamma, IL-1beta and TNFalpha were significantly higher in PD patients than in HC subjects (p<0.001), as determined by RT-PCR and Elisa methods. Cyto/chemokine levels were significantly correlated with UPDRS III and H/Y stage (p<0.001). The Pearson's correlation coefficient (R) was also used to assess the strength of the relationship between NF-kappaBp65 levels and all studied cyto/chemokines and between NF-kappaBp65, UPDRS III and H/Y score in PD patients. The overall results strengthen and extend the knowledge of the peripheral dysregulation in the cytokine network associated with PD.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Case-Control Studies
  • Chemokine CCL2 / blood
  • Chemokine CCL2 / genetics
  • Chemokine CCL3 / blood
  • Chemokine CCL3 / genetics
  • Chemokine CCL5 / blood
  • Chemokine CCL5 / genetics
  • Cytokines / blood
  • Cytokines / genetics*
  • Enzyme-Linked Immunosorbent Assay
  • Female
  • Gene Expression Profiling
  • Humans
  • Interferon-gamma / blood
  • Interferon-gamma / genetics
  • Interleukin-1beta / blood
  • Interleukin-1beta / genetics
  • Interleukin-8 / blood
  • Interleukin-8 / genetics
  • Leukocytes, Mononuclear / cytology
  • Leukocytes, Mononuclear / drug effects
  • Leukocytes, Mononuclear / metabolism*
  • Male
  • Middle Aged
  • Parkinson Disease / blood
  • Parkinson Disease / genetics
  • Parkinson Disease / pathology*
  • Polysaccharides / pharmacology
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Reverse Transcriptase Polymerase Chain Reaction
  • Tumor Necrosis Factor-alpha / blood
  • Tumor Necrosis Factor-alpha / genetics


  • CCL2 protein, human
  • Chemokine CCL2
  • Chemokine CCL3
  • Chemokine CCL5
  • Cytokines
  • Interleukin-1beta
  • Interleukin-8
  • Polysaccharides
  • RNA, Messenger
  • Tumor Necrosis Factor-alpha
  • Interferon-gamma