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Published on: July 16, 2019
[Interferon gamma concentration in the cerebrospinal fluid of patients with tick-borne encephalitis]
Maciej Kondrusik1, Joanna Zajkowska, Sławomir Pancewicz
1Klinika Chorób Zakaźnych i Neuroinfekcji, Akademia Medyczna w Białymstoku. mkondrusik@poczta.onet.pl
Insights
Interferon gamma (IFN-g) levels in cerebrospinal fluid are elevated in tick-borne encephalitis (TBE) patients early on, correlating with inflammation. IFN-g levels decrease post-treatment, indicating its role in TBE pathogenesis.
Area of Science:
- Neuroscience
- Immunology
- Infectious Diseases
Background:
- Tick-borne encephalitis (TBE) is a serious neurological disease.
- Understanding early disease markers is crucial for diagnosis and management.
Purpose of the Study:
- To measure interferon gamma (IFN-g) levels in cerebrospinal fluid (CSF) during early TBE and after treatment.
- To correlate IFN-g levels with disease severity and treatment response.
Main Methods:
- CSF samples from 40 TBE patients were analyzed using ELISA.
- Patients were categorized into mild, prolonged, severe TBE, and co-infected groups.
- CSF was examined at diagnosis and post-treatment.
Main Results:
- Significantly elevated CSF IFN-g was observed in all TBE groups compared to controls at diagnosis.
- CSF IFN-g levels decreased significantly after treatment in all groups.
- The highest initial IFN-g concentration was in patients with severe TBE.
Conclusions:
- CSF IFN-g concentration correlates with inflammation activity in early-stage TBE.
- No association was found between IFN-g levels and persistent CSF parameter increases.
Background And Purpose:
The purpose of this work was to evaluate interferon gamma (IFN-g) concentration in the cerebrospinal fluid of patients with diagnosed tick-borne encephalitis (TBE) early in the course of the disease and after the treatment.
Material And Methods:
The cerebrospinal fluid of 40 patients with TBE was examined. Patients were divided into 4 groups: group 1 consisted of 13 patients with mild clinical course, group 2 included 12 patients with prolonged TBE showing the presence of inflammatory markers after the treatment, group 3 comprised 9 patients with severe TBE presenting with disorders of consciousness and group 4 consisted of 6 patients with a simultaneous B. burgdorferi infection. The cerebrospinal fluid was examined twice--during TBE diagnosing and after the treatment. IFN-g was detected by the ELISA method.
Results:
The concentration of IFN-g in the cerebrospinal fluid in the first examination was significantly higher in all four groups of patients in comparison with controls. After the treatment, concentration of IFN-g decreased significantly in all studied groups. The highest concentration of IFN-g at the first examination was found in group 3. The concentration of IFN-g at the second examination was similar among 4 groups of patients and in controls.
Conclusions:
We found the correlation between IFN-g concentration in the cerebrospinal fluid of patients at the early stage of TBE and inflammation activity. We did not find any association between IFN-g concentration and a persistent increase of the cerebrospinal fluid parameters.
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