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Table of Contents
Vol. 8, No. 5, 2011
Issue release date: June 2011
Section title: Original Paper
Free Access
Neurodegenerative Dis 2011;8:375–380

Depletion of Plasma Gelsolin in Patients with Tick-Borne Encephalitis and Lyme Neuroborreliosis

Kułakowska A.a · Zajkowska J.M.b · Ciccarelli N.J.d · Mroczko B.c · Drozdowski W.a · Bucki R.d
Departments of aNeurology, bInfectious Diseases and Neuroinfections and cBiochemical Diagnostics, Medical University of Białystok, Białystok, Poland; dInstitute for Medicine and Engineering, University of Pennsylvania, Philadelphia, Pa., USA
email Corresponding Author

Robert Bucki

Institute for Medicine and Engineering, University of Pennsylvania

1010 Vagelos Research Laboratories, 3340 Smith Walk

Philadelphia, PA 19104 (USA)

Tel. +1 215 573 9787, E-Mail buckirob@mail.med.upenn.edu

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Background/Aims: Cell damage during the course of inflammation results in cytoplasmic actin release, which if not eliminated by the extracellular actin scavenger system, composed of gelsolin and vitamin D binding protein, can cause dysfunction of hemostasis and toxicity towards surrounding cells. In this study, we test the hypothesis that an inflammatory reaction induced by central nervous system infections such as tick-borne encephalitis (TBE) or Lyme neuroborreliosis (LNB) will result in plasma gelsolin concentration changes in the blood and cerebrospinal fluid (CSF). Methods: Quantitative Western blot was used to determine gelsolin levels in 58 samples, which include: 29 patients without infection (diagnosed with conditions such as idiopathic cephalalgia, idiopathic Bell’s facial nerve palsy and ischialgia due to discopathy in which standard CSF diagnostic tests show no abnormalities), 12 patients diagnosed with TBE, and 17 patients diagnosed with LNB sub forma meningitis. Results and Conclusion: The gelsolin concentration in the blood of patients with TBE (163.2 ± 80.8 µg/ml) and LNB (113.6 ± 56.8 µg/ml) was significantly lower (p < 0.05 and p < 0.001, respectively) compared to the control group (226.3 ± 100.7 µg/ml). Furthermore, there was no statistically significant difference between the CSF gelsolin concentration in patients with TBE (3.9 ± 3.3 µg/ml), LNB (2.9 ± 1.2 µg/ml) and the control group (3.7 ± 3.3 µg/ml). An observed decrease in gelsolin concentration in the blood of TBE and LNB patients supports previous findings indicating the involvement of gelsolin in the pathophysiology of an inflammatory response. Therefore, evaluation of blood gelsolin concentration and administration of recombinant plasma gelsolin might provide a new tool to develop diagnostic and therapeutic strategies for TBE and LNB.

© 2011 S. Karger AG, Basel

Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: September 28, 2010
Accepted: January 13, 2011
Published online: March 10, 2011
Issue release date: June 2011

Number of Print Pages: 6
Number of Figures: 1
Number of Tables: 1

ISSN: 1660-2854 (Print)
eISSN: 1660-2862 (Online)

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