Please use this identifier to cite or link to this item: http://hdl.handle.net/20.500.12857/115598
Title: Adenosine-mediated enteric neuromuscular function is affected during herpes simplex virus type 1 infection of rat enteric nervous system
Authors: Zoppellaro, Chiara 
Bin, Anna 
Brun, Paola 
Banzato, Serena
Macchi, Veronica 
Castagliuolo, Ignazio 
Giron, Maria Cecilia 
Keywords Plus: LONGITUDINAL MUSCLE;MYENTERIC MOTONEURONS;ORAL INOCULATION;GENE-EXPRESSION;MOUSE ILEUM;ECTO-ATPASE;RECEPTORS;A(1);A(2A);MODULATION
Mesh headings: Adenosine;Gastrointestinal Motility;Herpes Simplex;Herpesvirus 1, Human;Myenteric Plexus;Neuromuscular Junction;Vasodilator Agents
Secondary Mesh headings: Adenosine Deaminase;Animals;Chlorocebus aethiops;Male;Membrane Proteins;Rats;Rats, Wistar;Receptors, Purinergic;Vero Cells
Issue Date: 2013
Publisher: PUBLIC LIBRARY SCIENCE
Journal: PloS one 
Abstract: 
Adenosine plays an important role in regulating intestinal motility and inflammatory processes. Previous studies in rodent models have demonstrated that adenosine metabolism and signalling are altered during chronic intestinal inflammatory diseases. However, the involvement of the adenosinergic system in the pathophysiology of gut dysmotility associated to a primary neurodysfunction is still unclear. Recently, we showed that the neurotropic Herpes simplex virus type-1 (HSV-1), orally inoculated to rodents, infects the rat enteric nervous system (ENS) and affects gut motor function without signs of systemic infection. In this study we examined whether changes in purinergic metabolism and signaling occur during permanent HSV-1 infection of rat ENS. Using isolated organ bath assays, we found that contraction mediated by adenosine engagement of A1 or A2A receptors was impaired at 1 and 6 weeks post-viral administration. Immunofluorescence studies revealed that viral infection of ENS led to a marked redistribution of adenosine receptors: A1 and A2B receptors were confined to the muscle layers whereas A2A and A3 receptors were expressed mainly in the myenteric plexus. Viral-induced ENS neurodysfunction influenced adenosine metabolism by increasing adenosine deaminase and CD73 levels in longitudinal muscle-myenteric plexus with no sign of frank inflammation. This study provides the first evidence for involvement of the adenosinergic system during HSV-1 infection of the ENS. As such, this may represent a valid therapeutic target for modulating gut contractility associated to a primary neurodysfunction.
URI: http://hdl.handle.net/20.500.12857/115598
ISSN: 1932-6203
DOI: 10.1371/journal.pone.0072648
Appears in Collections:Articles

Show full item record

PubMed Central
Citations 50

11
Last Week
0
Last month
0
checked on Jul 15, 2021

SCOPUSTM   
Citations 50

13
checked on Sep 1, 2020

WEB OF SCIENCETM
Citations

19
checked on Nov 26, 2021

Page view(s) 20

1
checked on Nov 29, 2021

Google ScholarTM

Check

Altmetric


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.