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Immunocorrection of altered cytokine production in neurological patients
Author(s) -
Uchakina Olga N,
Uchakin Peter N,
Mezentseva Marina V,
Scherbenko Vahtang E,
Karabanov Alexey V,
IvanovaSmolenskaya Irina A,
Ershov Felix I
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.5.a1128-c
Subject(s) - cytokine , secretion , medicine , pathogenesis , immunology , immune system , in vitro , in vivo , interferon , endocrinology , pharmacology , biology , biochemistry , microbiology and biotechnology
Well established psycho‐neuro‐endocrine‐immune interactions play a significant role in the pathogenesis of neurological diseases. The major objective for this study was to investigate cytokine production and new approaches for immunocorrection in patients with Parkinson's (PD) and Wilson's diseases (WD). Cytokine profile was studied in 16 patients 5 times with 3‐month intervals (I, II, III, IV, V). Mitogen‐induced and plasma level of 8 cytokines, their gene expression in the peripheral immunocompetent cells, and response of immunocytes to recombinant interferons, interferon‐inducing chemicals and the nootropic drug Semax were assessed. Plasma level of IL‐6 significantly decreased 36% at the interval V in WD patients. Significant difference in plasma IL‐12 was observed between PD and WD patients at the interval V. Significant decrease of interferon (IFN)‐γ secretion in vitro was observed at interval III. In vitro secretion of IFN‐α was significantly lower at II and III intervals vs. I interval (8.0±2.1U/ml, and 10.8±2.4U/ml vs. 24.0±3.6U/ml) in PD patients Pretreatment of cells with exogenous IFN‐α did not affect secretion of endogenous IFN in cell cultures at the interval I, but recovered its diminished secretion in vitro at the interval III. Similar pattern in IFN secretion was observed in the Semax‐treated cultures. Data revealed alterations in the interferon system which may increase risk of neurological patients for the viral infections.