Anti-Enteric Neuronal Antibodies and the Irritable Bowel Syndrome.
- Author:
Jackie D WOOD
1
;
Sumei LIU
;
Douglas A DROSSMAN
;
Yehuda RINGEL
;
William E WHITEHEAD
Author Information
1. Department of Physiology and Cell Biology, The Ohio State University Medical Center, Columbus, Ohio, USA. wood.13@osu.edu
- Publication Type:Original Article
- Keywords:
Autoimmune neuropathy;
Enteric nervous system;
Gastrointestinal disorders
- MeSH:
Abdominal Pain;
Antibodies;
Autoantigens;
Cytoplasm;
Defecation;
Enteric Nervous System;
Gastrointestinal Diseases;
Humans;
Irritable Bowel Syndrome;
Neurons;
North Carolina;
Physical Processes;
Protein Array Analysis;
Ribonucleoproteins;
Rome
- From:Journal of Neurogastroenterology and Motility
2012;18(1):78-85
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND/AIMS: Functional gastrointestinal disorders are those in which no abnormal metabolic or physical processes, which can account for the symptoms, can be identified. The irritable bowel syndrome (IBS) is a significant functional disorder, which affects 10-20 percent of the population worldwide. Predominant symptoms of IBS are abnormal defecation associated with abdominal pain, both of which may be exacerbated by psychogenic stress. Our study was designed to test a hypothesis that symptoms in a subset of patients with a diagnosis of IBS are associated with an autoimmune degenerative neuropathy in the enteric nervous system. METHODS: Serum was collected from Rome II-IBS patients and controls at the University of North Carolina Functional Gastrointestinal Diseases Center. Assay procedures were immunohistochemical localization of antibody binding to enteric neurons and human protein microarray assay for antigens recognized by antibodies in the sera. RESULTS: Eighty-seven percent of IBS sera and 59% of control sera contained anti-enteric neuronal antibodies. Antibody immunostaining was seen in the nucleus and cytoplasm of neurons in the enteric nervous system. Protein microarray analysis detected antibody reactivity for autoantigens in serum with anti-enteric neuronal antibodies and no reactivity for the same autoantigens in samples not containing anti-enteric neuronal antibodies in our immunostaining assay. Antibodies in sera from IBS patients recognized only 3 antigens out of an 8,000 immunoprotein array. The 3 antigens were: (1) a nondescript ribonucleoprotein (RNP-complex); (2) small nuclear ribonuclear polypeptide A; and (3) Ro-5,200 kDa. CONCLUSIONS: Results of the present study suggest that symptoms in a subset of IBS patients might be a reflection of enteric neuronal damage or loss, caused by circulating anti-enteric autoimmune antibodies.
