Neuronal Protein Alteration in Enteric Dysmotility Syndrome

Little is known about the enteric ganglionic system in subjects with gastrointestinal dysmotility syndrome (GIDS). Furthermore, dysfunction of gastrointestinal motility is an early complaint of subjects with Parkinson’s disease. Here, we assessed p62/sequestosome-1(p62) and α-synuclein (αS) immunoreactivity (IR) in full-thickness bowel specimens of the gut obtained from six subjects with GIDS and from 17 controls. In the myenteric neurons, fine punctuate p62-IR were seen in all of the controls, whereas diffuse cytoplasmic and nuclear p62-IR were seen in the GIDS cases. Physiological αS-IR (clone 42/αS) was seen in all of the controls and the GIDS cases in the lamina propria, the submucosal and in the myenteric plexuses. The disease associated αS (clone 5G4) labeled the cytoplasm of the ganglion cells only in the myenteric plexus in three out of the four subjects with the GIDS/inflammatory neuropathy. In summary, ganglion cells were readily visualized in all of the layers of the bowel with clone 42/αS, and p62 displayed altered patterns of labeling in subjects with the GIDS. Labeling seen with the disease associated clone 5G4/αS in the GIDS/inflammatory neuropathy is intriguing and might indicate that the alteration of αS is triggered by a chronic inflammation. *Corresponding author: Irina Alafuzoff, Department of Immunology, Genetics and Pathology, Uppsala University Hospital, Rudbeck Laboratory, Dag Hammarskjölds väg 20, 751 85, Uppsala, Sweden. Tel: +46 (0) 706114822; E-mail: [email protected] Received January 08, 2016; Accepted February 10, 2016; Published February 16, 2016 Citation: Alafuzoff I, Popova SN, Wanders A, Veress B (2016) Neuronal Protein Alteration in Enteric Dysmotility Syndrome. J Alzheimers Dis Parkinsonism 6: 212. doi: 10.4172/2161-0460.1000212 Copyright: © 2016 Alafuzoff I, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. 2009 Working Group and is primarily based on hematoxylin-eosin (HE) stained sections [1]. New 4 μm thick sections were prepared from all of the cases for this study. None of the subjects had shown any signs or symptoms of a cerebral ND. The study was approved by the Uppsala Ethical Committee Dnr 2011/023 and 2011/289 Immunohistochemistry For p62-IR, clone GP62-C was used (Progen Biotechnik GmbH, Heidelberg, Germany) at a dilution ratio of 1:100, pre-treatment autoclave 120°C in Ultra CCI Tris buffer, and the IHC staining was carried out in a BenchMark Ultra instrument (Ventana Medical Systems, Inc., Tucson, AZ). For detection, the peroxidase-conjugated streptavidin-biotin method was used (Dako Cytomation, Glostrup, Denmark) with DAB as chromogen. For physiological αS-IR, clone 42/ αS (BD Transduction Laboratories, Franklin Lakes, NJ) and for disease associated αS clone 5G4/αS (Analytic Jena AG, Jena, Germany) were used at a dilution ratio of 1:1000, pre-treatment autoclave 120°C in citrate buffer, pH 6.0 followed by 5 min in 80% formic acid, and the IHC staining was carried out manually. For detection, Histostain®-Plus 3rd generation IHC detection Kit (Invitrogen, Carlsbad, CA) was used with Romulin AEC chromogen (Biocare Medical, Concord, CA). Citation: Alafuzoff I, Popova SN, Wanders A, Veress B (2016) Neuronal Protein Alteration in Enteric Dysmotility Syndrome. J Alzheimers Dis Parkinsonism 6: 212. doi: 10.4172/2161-0460.1000212