Immunology Letters 185 (2017) 93–97 Contents lists available at ScienceDirect Immunology Letters j ourna l ho me page: www.elsevier.com/locate/immlet sNCAM as a specific marker of peripheral demyelination  Adam Niezgoda a,∗ , Sławomir Michalak b,c , Jacek Losy c,d , Alicja Kalinowska-Lyszczarz a , Wojciech Kozubski a a Chair and Department of Neurology, Poznan University of Medical Sciences, Pozna´ n, ul. Przybyszewskiego 49 Pozna´ n, 60-355, Poland b Department of Neurochemistry and Neuropathology, Poznan University of Medical Sciences, Pozna´ n, ul. Przybyszewskiego 49, Pozna´ n, 60-355, Poland c Neuroimmunological Unit, Miroslaw Mossakowski Medical Research Center of the Polish Academy of Sciences, Pozna´ n, ul. Przybyszewskiego 49, Pozna´ n, 60-355, Poland d Department of Neuroimmunology, Chair of Neurology Poznan University of Medical Sciences, Pozna´ n, ul. Przybyszewskiego 49, Pozna´ n, 60-355, Poland a r t i c l e i n f o Article history: Received 20 October 2016 Accepted 15 March 2017 Available online 21 March 2017 Keywords: Adhesion molecules NCAM Demyelinating polyneuropathy Axonal polyneuropathy Peripheral nerve inflammation Electroneurography ELISA immune assay Overall Neuropathy Limitations Scale a b s t r a c t Adhesion molecules are involved in nerve growth, synaptic plasticity and myelin formation and main- tenance process. Neural cell adhesion molecule (CD56 or NCAM) seems to play a crucial role in all the above-mentioned events. Having found poly-sialylated NCAM increased re-expression on demyelinated axons within multiple sclerosis plaques we assessed soluble NCAM (sNCAM) in sera of patients with various types of peripheral nerve affections - demyelinating, axonal “inflammatory”, axonal metabolic polyneuropathies and healthy controls. These data were compared with the clinical state using Overall Neuropathy Limitations Scale (ONLS) and nerve conduction studies. We found significantly increased sNCAM concentration in demyelinating polyneuropathies in comparison to axonal group and healthy controls as well as significantly increased sNCAM level in axonal group in comparison to healthy sub- jects. We also found high positive correlation between sNCAM and ONLS and strong negative correlation between sNCAM level and the lowest conduction velocity (V min ) found in a patient. We conclude that sNCAM might be thought as a specific marker of peripheral nerve demyelination and as a sensitive marker of peripheral nerve injuries. © 2017 European Federation of Immunological Societies. Published by Elsevier B.V. All rights reserved. 1. Introduction Adhesion molecules are involved in nerve growth, re-growth, synaptic plasticity, cognitive functions as well as in the process of myelin formation and its maintenance. Neural cell adhesion molecule (CD56 or NCAM) seems to play a crucial role in all the above-mentioned events. NCAM is a member of the immunoglobulin (Ig) superfamily expressed on the surface of several types of neural cells and its ubiquitous presence in the nervous system has been documented across species [1]. It is involved in cell-to-cell interactions dur- ing brain development, regeneration and synaptic modeling [2–5]. NCAM can act homophilically with another NCAM and was first identified by this function [6]. It may also interact by heterophili- cal adhesion with other molecules like L1 [7], signal transduction molecules [8], cytoskeletal components [9], laminin [10].  This work was supported by Chair of Neurology, University of Medical Sciences, Pozna ´ n, Poland. ∗ Corresponding author. E-mail address: adamniezgoda@wp.pl (A. Niezgoda). Neural cell adhesion molecule is a glycoprotein coded by a 70 kb single gene localized by Cunningham et al. [11] to human chromo- some 11; the molecule has an intracellular, transmembrane and extracellular portion. The final product of the NCAM gene becomes polysialylated in its extracellular part and may appear in more than 20 different isoforms (e.g. 120, 140 i 180 kDa). Like other adhesion molecules NCAM may appear as a soluble form (sNCAM) - which is cleaved of the cell surface from its cell-bound form. It is generally believed that posttranslational polysialylation gives NCAM (PSA-NCAM) high flexibility in its extracellular por- tion made of five immunoglobulin and two fibronectin domains which is necessary for space orientation changes and close con- tact with other cells [12]. Polysialylation of NCAM is assured by two different enzymes. It is assumed that PSA chain increases elasticity, cell mobility or diffusion by decreasing NCAM–NCAM or NCAM-nonNCAM (e.g.NCAM-cytoskeleton) adhesion [13]; [14]. PSA-NCAM is present on immature non-myelinated axons and neg- atively correlates with the progress of myelination. As described Nait-Oumesmar et al. [15] it may reappear on denuded demyeli- nated axons, that is why it has been called the “young” or “embryonic” form of NCAM. http://dx.doi.org/10.1016/j.imlet.2017.03.011 0165-2478/© 2017 European Federation of Immunological Societies. Published by Elsevier B.V. All rights reserved.