Infectious agents as potential triggers for autoimmunity in achalasia

Furuzawa‐Carballeda, Janette; Coss‐Adame, Enrique; Valdovinos, Miguel A.; Aguilar‐León, Diana; Torres‐Villalobos, Gonzalo

doi:10.24875/ngl.19000044

Cited by 2 publications

(3 citation statements)

References 79 publications

(143 reference statements)

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“… 7 Viral infections, especially chronic latent and active infections caused by neurotropic viruses with a preference for squamous epithelium, could be a triggering factor in the chronic inflammatory process of the myenteric plexus of the esophagus in genetically predisposed subjects. 6 , 8 Proposed candidate viruses have included herpes simplex virus (HSV), varicella Zoster virus, Measles virus, human papillomavirus, “JC” virus, mumps, and bornavirus. The association of achalasia with other viruses such as Cytomegalovirus, Epstein–Barr virus, 6 , 8 or Coronaviruses has not been reported in the literature.…”

Section: Introductionmentioning

confidence: 99%

“… 6 , 8 Proposed candidate viruses have included herpes simplex virus (HSV), varicella Zoster virus, Measles virus, human papillomavirus, “JC” virus, mumps, and bornavirus. The association of achalasia with other viruses such as Cytomegalovirus, Epstein–Barr virus, 6 , 8 or Coronaviruses has not been reported in the literature. However, there is a high susceptibility to infection of the gastrointestinal tract by SARS‐CoV‐2 due to the expression of the receptor for angiotensin‐converting enzyme type II (ACE2) in ileal epithelial cells (~30% ACE2‐positive cells) and esophagus epithelial cells (>1% ACE2‐positive cells).…”

Section: Introductionmentioning

confidence: 99%

“…It could be important for developing an aberrant immune response secondary to initiates such as viral or bacterial infections 7 . Viral infections, especially chronic latent and active infections caused by neurotropic viruses with a preference for squamous epithelium, could be a triggering factor in the chronic inflammatory process of the myenteric plexus of the esophagus in genetically predisposed subjects 6,8 . Proposed candidate viruses have included herpes simplex virus (HSV), varicella Zoster virus, Measles virus, human papillomavirus, “JC” virus, mumps, and bornavirus.…”

Section: Introductionmentioning

confidence: 99%

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Is the Sars‐CoV‐2 virus a possible trigger agent for the development of achalasia?

Furuzawa‐Carballeda

Icaza-Chávez²,

Aguilar‐León

et al. 2022

Neurogastroenterology Motil

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Background Achalasia is an autoimmune disease whose probable causal agent is a neurotropic virus that chronically infects the myenteric plexus of the esophagus and induces the disease in a genetically susceptible host. The association between achalasia and coronaviruses has not been reported. Aims To evaluate the presence of the SARS‐CoV‐2 virus, the ACE2 expression, the tissue architecture, and immune response in the lower esophageal sphincter muscle (LESm) of achalasia patients who posteriorly had SARS‐CoV‐2 (achalasia‐COVID‐19) infection before laparoscopic Heller myotomy (LHM) and compare the findings with type II achalasia patients and transplant donors (controls) without COVID‐19. Methods The LESm of 7 achalasia‐COVID‐19 patients (diagnosed by PCR), ten achalasia patients, and ten controls without COVID‐19 were included. The presence of the virus was evaluated by in situ PCR and immunohistochemistry. ACE2 receptor expression and effector CD4 T cell and regulatory subsets were determined by immunohistochemistry. Key Results Coronavirus was detected in 6/7 patients‐COVID‐19. The SARS‐CoV‐2 was undetectable in the LESm of the achalasia patients and controls. ACE2 receptor was expressed in all the patients and controls. One patient developed achalasia type II post‐COVID‐19. The percentage of Th22/Th17/Th1/pDCreg was higher in achalasia and achalasia‐COVID‐19 pre‐HLM vs. controls. The Th2/Treg/Breg cell percentages were higher only in achalasia vs. controls. Conclusion & Inferences SARS‐CoV2 and its receptor expression in the LESm of achalasia patients who posteriorly had COVID‐19 but not in the controls suggests that it could affect the myenteric plexus. Unlike achalasia, patients‐COVID‐19 have an imbalance between effector CD4 T cells and the regulatory mechanisms.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Is the Sars‐CoV‐2 virus a possible trigger agent for the development of achalasia?

Furuzawa‐Carballeda

Icaza-Chávez²,

Aguilar‐León

et al. 2022

Neurogastroenterology Motil

Self Cite

View full text Add to dashboard Cite

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Is the Sars-CoV-2 virus a possible trigger agent for the development of achalasia?

Furuzawa‐Carballeda

Icaza-Chávez²,

Aguilar‐León

et al. 2022

Preprint

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Introduction: Previous studies have suggested that achalasia is an autoimmune disease whose probable causal agent is a neurotropic virus that chronically infects the myenteric plexus of the esophagus and, in a genetically susceptible host, induces the disease. The association between achalasia and coronaviruses has not been reported in the literature. Objective: To evaluate the presence of the SARS-CoV-2 virus, the ACE2 expression, the tissue architecture, and immune response in the lower esophageal sphincter (LES) muscle of patients with achalasia who had SARS-CoV-2 infection before laparoscopic Heller myotomy (LHM) and compare the findings with patients with type II achalasia and transplant donors (controls) without COVID-19. Material and Methods: The LES muscle of 7 patients with achalasia who had SARS-CoV-2 infection before LHM (diagnosed by PCR), ten patients with achalasia, and ten transplant donors (controls) without COVID-19 were included. The presence of the virus was evaluated by in situ PCR and immunohistochemistry. ACE2 receptor expression and CD4 T cell and regulatory subsets were determined by immunohistochemistry. Results: All patients had type II achalasia. Coronavirus was detected in 6/7 patients who had COVID-19. The SARS-CoV-2 was undetectable in the LES muscle of the achalasia patients and transplant donors (controls). The ACE2 receptor was expressed in all the patients and controls. One patient developed achalasia type II post-COVID-19. The percentage of Th22, Th17, Th1, and pDCreg was higher in achalasia and achalasia-COVID-19 pre-HLM vs. transplant donors. The Th2, Treg, and Breg cell percentages were higher only in achalasia vs. transplant donors. Conclusion: The presence of the SARS-CoV2 and its receptor in the LES muscle of patients with type II achalasia who had COVID-19 pre-LHM but not in the controls suggests that it could affect the myenteric plexus. Unlike patients with achalasia, patients who had COVID-19 have an imbalance between effector CD4 T cells and the regulatory mechanisms.

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Infectious agents as potential triggers for autoimmunity in achalasia

Cited by 2 publications

References 79 publications

Is the Sars‐CoV‐2 virus a possible trigger agent for the development of achalasia?

Is the Sars‐CoV‐2 virus a possible trigger agent for the development of achalasia?

Is the Sars-CoV-2 virus a possible trigger agent for the development of achalasia?

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