Aberrated levels of cerebrospinal fluid chemokines in Guillain-Barré syndrome and chronic inflammatory demyelinating polyradiculoneuropathy.
Infiltration of spinal nerve roots and peripheral nerves by macrophages and T cells are rather consistent immunopathologic findings in patients with Guillain-Barré syndrome (GBS) and chronic inflammatory demyelinating polyradiculoneuropathy (CIDP). Chemokines play a central role in recruitment of leukocytes to inflamed tissue. Chemokines have been implicated in the pathogenesis of the experimental autoimmune neuritis (EAN), which represents an animal model of GBS, but the role of chemokines in GBS and CIDP is not clear. Since chemokines may be released into CSF from inflamed spinal nerve roots, we studied the concentrations of the chemokines MCP-1, MIP-1beta, MIP-3beta, IP-10, SDF-1alpha, RANTES, and SLC in the CSF by sandwich ELISA in patients over the course of GBS and CIDP, before and after immunomodulatory treatment. Controls consisted of patients with noninflammatory neurological disorders. Patients examined in the acute phase of GBS prior to treatment with intravenous high dose immunoglobulins (IvIg) had elevated CSF levels of MCP-1 (a chemoattractant for blood monocytes and dendritic cells) and IP-10 (a chemoattractant for T cells). Patients with CIDP examined prior to immunomodulatory treatment had elevated CSF levels of MIP-3beta (a chemoattractant for mature dendritic cells, naïve and recently activated T cells) and IP-10. Levels of MIP-3beta tended to decreased during follow-up in those CIDP patients responding favorably to immunomodulatory treatment. CSF levels of MCP-1 and IP-10 correlated with the CSF:plasma albumin ratio in both GBS and CIDP patients. In CIDP patients, CSF levels of MIP-3beta also correlated with the CSF:plasma albumin ratio. These data implicate MCP-1 and IP-10 in the pathogenesis of GBS, and IP-10 and MIP-3beta in the pathogenesis of CIDP.
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Neuroimmunology Unit, Neurotec Department, Karolinska Institutet and Department of Neurology, Huddinge University Hospital, Stockholm, Sweden. rayomand.press@neurotec.ki.se
Pashenkov
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Jin
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D000328:Adult; D054415:Chemokine CCL19; D018932:Chemokine CCL2 / Q000097:blood / Q000134:cerebrospinal fluid; D054357:Chemokine CXCL10 / Q000097:blood; D018925:Chemokines / Q000097:blood / Q000134:cerebrospinal fluid*; D019742:Chemokines, CC / Q000097:blood / Q000134:cerebrospinal fluid; D018450:Disease Progression; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D020275:Guillain-Barre Syndrome / Q000097:blood / Q000134:cerebrospinal fluid* / Q000188:drug therapy / Q000276:immunology*; D006801:Humans; D016756:Immunoglobulins, Intravenous / Q000627:therapeutic use; D008297:Male; D008776:Methylprednisolone Hemisuccinate / Q000627:therapeutic use; D008875:Middle Aged; D020277:Polyradiculoneuropathy, Chronic Inflammatory Demyelinating / Q000134:cerebrospinal fluid* / Q000188:drug therapy / Q000276:immunology*
C515460:CCL19 protein, human; D054415:Chemokine CCL19; D018932:Chemokine CCL2; D054357:Chemokine CXCL10; D018925:Chemokines; D019742:Chemokines, CC; D016756:Immunoglobulins, Intravenous; D008776:Methylprednisolone Hemisuccinate