Evaluation of NF-κB concentration in patients with tick-borne encephalitis, neuroborreliosis, anaplasmosis and Anaplasma phagocythophilum with tick-borne encephalitis virus co-infection. (February 2017)

• Record Type: Journal Article
• Authors: Moniuszko-Malinowska, Anna; Czupryna, Piotr; Dunaj, Justyna; Swierzbinska, Renata; Guziejko, Katarzyna; Rutkowski, Ryszard; Zajkowska, Joanna; Grygorczuk, Sambor; Kondrusik, Maciej; Pancewicz, Sławomir
• Is Part Of: Cytokine. Volume 90(2017)
• Page Start: 155
• Page End: 160
• Publication Date: 2017-02
• Subjects: NF-κB -- Tick-borne diseases -- Co-infection; Cytokines -- Periodicals; 571.844
• DOI: 10.1016/j.cyto.2016.10.014
• Languages: English
• ISSNs: 1043-4666

Abstract

Highlights: NF-κB increases in cerebrospinal fluid (CSF) during nervous system inflammation. Tick-borne encephalitis with anaplasmosis (TBE + ANA) increases NF-κB in serum. Serum NF-κB concentration differentiates TBE + ANA with TBE and neuroborreliosis. Serum and CSF NF-κB concentration may monitor tick-borne encephalitis treatment. Cerebrospinal fluid NF-κB concentration may monitor neuroborreliosis treatment. Abstract: Objectives: The aim of the study was the evaluation of NF-κB concentration in serum and cerebrospinal fluid (CSF) of patients with diagnosis of tick-borne diseases: tick-borne encephalitis (TBE), neuroborreliosis (NB), anaplasmosis (ANA) and patients co-infected with tick-borne encephalitis virus and Anaplasma phagocythophilum (TBE + ANA). Additionally NF-κB concentration during acute and convalescent period was compared. Methods: Sixty-seven patients with diagnosis of tick-borne diseases were included in the study. The control group (CG) consisted of 18 patients hospitalized because of headaches and had lumbar puncture performed. The NF-κB was measured by human inhibitory subunit of NF-κB ELISA Kit during acute and convalescent period. Results: In serum the significant differences were observed only in patients with TBE + ANA co-infection. In CSF the concentration of NF-κB was significantly higher in patients with TBE, TBE + ANA co-infection, and patients with NB than in CG. Receiver operating characteristic (ROC) curves analysis showed that NF-κB concentration in CSF differentiated patients with NB with CG; patients co-infected with TBE and ANA with CG and patients with TBE with CG. NF-κB concentration in serum differentiated patients co-infected with TBE and ANA with NB and with ANA, with TBE and with CG. In TBE group the serum NF-κB concentration significantly decreased in convalescent period, while in NB and TBE groups significant CSF decrease of NF-κB concentration was observed. Conclusions: 1. Inflammatory process in the CNS results in the increase of NF-κB concentration in CSF, due to the damage of blood-brain barrier. 2. Co-infection of TBE + ANA increases NF-κB concentration in serum. 3. NF-κB concentration in serum may be useful in the differentiation of TBE + ANA co-infection with TBE and NB. 4. NF-κB concentration may be used to monitor TBE and NB treatment effectiveness.