PURPOSE: Chemokines, including a chemoattractant for mononuclear cells CCL3 (MIP-1alpha), are responsible for attracting leukocytes into central nervous system (CNS) and cerebrospinal fluid (CSF) in meningitis and encephalomeningitis. We investigated the possibility of the involvement of CCL3 in tickborne encephalitis (TBE) pathogenesis. MATERIAL AND METHODS: We studied 26 patients with TBE; 13 with meningitis (group I) and 13 with encephalomeningits (group II). Control group included 11 patients without infectious disease of the CNS. CCL3 concentration was measured by ELISA in serum and CSF on admission (examination 1) and after 2 weeks (examination 2) in TBE patients and once in controls. RESULTS: In all control samples CCL3 concentration was below detection limit. In TBE, CCL3 serum concentration was: in group I--10.1 +/- 4.1 (mean +/- SD, ng/ml) in examination 1 and 12.4 +/- 4.8 in examination 2, and in group II--12.5 +/- 3.9 and 13.5 +/- 4.8, respectively. In CSF, CCL3 was detected: in group I in 5 patients in examination 1 (178 +/- 236 pg/ml) and 11 in examination 2 (457 +/- 215), in group II--in 8 (357 +/- 311) and 7 patients (326 +/- 330), respectively. There were no differences between group I and II. The comparison of CCL3 concentration gradient with albumin gradient between serum and CSF supported the possibility of intrathecal synthesis of CCL3. CONCLUSIONS: 1) Synthesis of CCL3, perhaps including intrathecal synthesis, is increased in TBE. 2) CCL3 concentration was much lower in CSF than in serum of the TBE patients, which argues against its significant role as chemoattractant in this condition.
PURPOSE: Chemokines, including a chemoattractant for mononuclear cells CCL3 (MIP-1alpha), are responsible for attracting leukocytes into central nervous system (CNS) and cerebrospinal fluid (CSF) in meningitis and encephalomeningitis. We investigated the possibility of the involvement of CCL3 in tickborne encephalitis (TBE) pathogenesis. MATERIAL AND METHODS: We studied 26 patients with TBE; 13 with meningitis (group I) and 13 with encephalomeningits (group II). Control group included 11 patients without infectious disease of the CNS. CCL3 concentration was measured by ELISA in serum and CSF on admission (examination 1) and after 2 weeks (examination 2) in TBE patients and once in controls. RESULTS: In all control samples CCL3 concentration was below detection limit. In TBE, CCL3 serum concentration was: in group I--10.1 +/- 4.1 (mean +/- SD, ng/ml) in examination 1 and 12.4 +/- 4.8 in examination 2, and in group II--12.5 +/- 3.9 and 13.5 +/- 4.8, respectively. In CSF, CCL3 was detected: in group I in 5 patients in examination 1 (178 +/- 236 pg/ml) and 11 in examination 2 (457 +/- 215), in group II--in 8 (357 +/- 311) and 7 patients (326 +/- 330), respectively. There were no differences between group I and II. The comparison of CCL3 concentration gradient with albumin gradient between serum and CSF supported the possibility of intrathecal synthesis of CCL3. CONCLUSIONS: 1) Synthesis of CCL3, perhaps including intrathecal synthesis, is increased in TBE. 2) CCL3 concentration was much lower in CSF than in serum of the TBE patients, which argues against its significant role as chemoattractant in this condition.
Authors: Petra Pokorna Formanova; Martin Palus; Jiri Salat; Vaclav Hönig; Michal Stefanik; Pavel Svoboda; Daniel Ruzek Journal: J Neuroinflammation Date: 2019-11-07 Impact factor: 8.322