title: [Concentration of the beta-chemokine CCL5 (RANTES) in cerebrospinal fluid in patients with tick-borne encephalitis].
abstract: OBJECTIVE
  In tick-borne encephalitis (TBE), perivascular infiltrates are formed within the central nervous system (CNS) and are accompanied by pleocytosis with a predominance of T CD4+ lymphocytes in cerebrospinal fluid (CSF). Factors responsible for leukocyte flow into CNS in TBE have not been investigated. We evaluated the concentration of the chemotactic factor for lymphocytes, chemokine CCL5 (RANTES, Regulated upon Activation, Normal T cell Expressed and Secreted) in CSF and serum of patients with TBE and assessed its correlation with CSF pleocytosis.
  
  
  METHODS
  Group I consisted of 10 patients with TBE virus infection presenting as meningitis; group II included 11 patients with TBE presenting as encephalomeningitis or myeloencephalomeningitis. The control group consisted of 8 patients, in whom neuroinfection and infection with TBE virus was excluded. The concentration of CCL5 was measured by ELISA in CSF and serum samples taken within 24 hours after hospitalization (examination 1) and in the convalescence period, on average after 16 days (examination 2).
  
  
  RESULTS
  Mean CCL5 concentration in serum did not differ between the groups, while in CSF it was significantly increased in group I (64.3+/-75.5 pg/ml in examination 1 and 44.4+/-39.5 pg/ml in examination 2) and in group II (38.4+/-17.0 pg/ml in examination 1 and 48.8+/-24.7 pg/ml in examination 2) in comparison with controls (3.7+/-5.3 pg/ml). There was no significant difference regarding CCL5 concentration between groups I and II and between the examination 1 and 2. There was no correlation between the concentration of CCL5 and CSF parameters.
  
  
  CONCLUSIONS
  The concentration of CCL5 is increased in CSF, but not in serum of patients with TBE. This increase does not depend on the clinical form of the disease and is sustained after the disappearance of the symptoms of acute infection. Further studies are necessary to determine the source of CCL5, and its role in the pathogenesis of TBE and its sequelae.
authors.affiliation: Klinika Chorób Zakaźnych i Neuroinfekcji, Akademia Medyczna, ul. Zurawia 14, 15-540 Białystok. neuroin@amb.edu.pl
authors.forename: Sambor
authors.initials: S
authors.lastname: Grygorczuk
authors.forename: Joanna
authors.initials: J
authors.lastname: Zajkowska
authors.forename: Renata
authors.initials: R
authors.lastname: Swierzbińska
authors.forename: Sławomir
authors.initials: S
authors.lastname: Pancewicz
authors.forename: Maciej
authors.initials: M
authors.lastname: Kondrusik
authors.forename: Teresa
authors.initials: T
authors.lastname: Hermanowska-Szpakowicz
mesh_terms: D000328:Adult; D000368:Aged; D015415:Biomarkers / Q000097:blood / Q000134:cerebrospinal fluid; D018946:Chemokine CCL5; D019742:Chemokines, CC / Q000097:blood / Q000134:cerebrospinal fluid*; D004675:Encephalitis, Tick-Borne / Q000097:blood / Q000134:cerebrospinal fluid* / Q000175:diagnosis; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006801:Humans; D008297:Male; D008587:Meningitis, Viral / Q000134:cerebrospinal fluid / Q000276:immunology; D008590:Meningoencephalitis / Q000134:cerebrospinal fluid / Q000276:immunology; D008875:Middle Aged
chemical_list: D015415:Biomarkers; C483024:CCL5 protein, human; D018946:Chemokine CCL5; D019742:Chemokines, CC