Infectious agents as potential triggers for autoimmunity in achalasia | Neurogastro Latam Reviews



Infectious agents as potential triggers for autoimmunity in achalasia



Janette Furuzawa-Carballeda, Department of Immunology and Rheumatology, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico City, Mexico
Enrique Coss-Adame, Departamento de Gastroenterología y Laboratorio de Motilidad Gastrointestinal, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Ciudad de México, México
Miguel A. Valdovinos, Departamento de Gastroenterología, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Ciudad de México, México
Diana Aguilar-León, Department of Experimental Pathology, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico City, Mexico
Gonzalo Torres-Villalobos, Departments of Experimental Surgery, and Surgery, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico City, Mexico


Idiopathic achalasia is an archetype espohageal motor disorder. It is an inflammatory disease caused by the loss of the inhibitory neurons of the esophageal myenteric plexus of unknown etiology. It is possible to postulate an etiopathogenic and physiopathogenic mechanism for achalasia. Initial event that triggers disease appears to be the result of a repetitive insult produced by a neurotropic infectious agent, which induces a persistent inflammation at the Auerbach’s plexus. Not all infected patients develop achalasia. Thus, only those individuals with genetic predisposition to develop an aggressive chronic inflammatory response will progress to the disease. Moreover, in most of the cases pathology is accompanied by the presence of neuronal antibodies that contribute to the destruction of the myenteric plexus. In this review, we will focus on the evaluation of the several aspects that suggest that achalasia is an autoimmune disease associated with a viral infection.



Keywords: Achalasia. Herpes simplex virus. Varicella zoster. Autoimmunity. Inflammation.