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Journal of Immunology Research
Volume 2015, Article ID 729217, 18 pages
http://dx.doi.org/10.1155/2015/729217
Research Article

Achalasia—An Autoimmune Inflammatory Disease: A Cross-Sectional Study

1Department of Immunology and Rheumatology, National Institute of Medical Sciences and Nutrition, Vasco de Quiroga No. 15, Colonia Sección XVI, 14000 Mexico City, DF, Mexico
2Department of Pathology, National Institute of Medical Sciences and Nutrition, Vasco de Quiroga No. 15, Colonia Sección XVI, 14000 Mexico City, DF, Mexico
3Department of Gastroenterology, National Institute of Medical Sciences and Nutrition, Vasco de Quiroga No. 15, Colonia Sección XVI, 14000 Mexico City, DF, Mexico
4Department of Experimental Surgery, National Institute of Medical Sciences and Nutrition, Vasco de Quiroga No. 15, Colonia Sección XVI, 14000 Mexico City, DF, Mexico

Received 15 January 2015; Revised 24 March 2015; Accepted 14 April 2015

Academic Editor: Ghislain Opdenakker

Copyright © 2015 J. Furuzawa-Carballeda et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Idiopathic achalasia is a disease of unknown etiology. The loss of myenteric plexus associated with inflammatory infiltrates and autoantibodies support the hypothesis of an autoimmune mechanism. Thirty-two patients diagnosed by high-resolution manometry with achalasia were included. Twenty-six specimens from lower esophageal sphincter muscle were compared with 5 esophagectomy biopsies (control). Immunohistochemical (biopsies) and flow cytometry (peripheral blood) analyses were performed. Circulating anti-myenteric autoantibodies were evaluated by indirect immunofluorescence. Herpes simplex virus-1 (HSV-1) infection was determined by in situ hybridization, RT-PCR, and immunohistochemistry. Histopathological analysis showed capillaritis (51%), plexitis (23%), nerve hypertrophy (16%), venulitis (7%), and fibrosis (3%). Achalasia tissue exhibited an increase in the expression of proteins involved in extracellular matrix turnover, apoptosis, proinflammatory and profibrogenic cytokines, and Tregs and Bregs versus controls (). Circulating Th22/Th17/Th2/Th1 percentage showed a significant increase versus healthy donors (). Type III achalasia patients exhibited the highest inflammatory response versus types I and II. Prevalence of both anti-myenteric antibodies and HSV-1 infection in achalasia patients was 100% versus 0% in controls. Our results suggest that achalasia is a disease with an important local and systemic inflammatory autoimmune component, associated with the presence of specific anti-myenteric autoantibodies, as well as HSV-1 infection.