Multisystem Inflammatory Syndrome and Autoimmune Diseases Following COVID-19: Molecular Mechanisms and Therapeutic Opportunities

Hosseini, Parastoo; Fallahi, Mohammad Sadegh; Erabi, Gisou; Pakdin, Majid; Zarezadeh, Seyed Mahdi; Faridzadeh, Arezoo; Entezari, Sarina; Ansari, Arina; Poudineh, Mohadeseh; Deravi, Niloofar

doi:10.3389/fmolb.2022.804109

Cited by 26 publications

(27 citation statements)

References 214 publications

(276 reference statements)

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“…Viruses are considered critical biological agents that cause autoimmunity with mechanisms such as molecular mimicry, bystander activation of T cells, transient immunosuppression, and inflammation, which has also been seen in post-COVID-19 autoimmunity. 22,23 In a previous study, our group has shown that most patients with achalasia have a latent and, in some cases, even active HSV-1 infection in the LES. 6 Additionally, Facco et al have identified an oligoclonal lymphocytic infiltrate within the LES of achalasia patients with the ability to recognize human HSV-1 antigens associated with an increased proliferation and Th1 type cytokines release.…”

Section: Discussionmentioning

confidence: 86%

Section: This Study Demonstrates the Plausibility Of Infection Of Eso...mentioning

confidence: 88%

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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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Section: Discussionmentioning

confidence: 86%

Section: This Study Demonstrates the Plausibility Of Infection Of Eso...mentioning

confidence: 88%

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

View full text Add to dashboard Cite

show abstract

“… 2 Moreover, it has been found that in addition to complications during illness, COVID‐19 patients are often observed to experience late‐onset complications, including interstitial pneumonia, cytopenia, arthralgia, myocarditis, and autoimmune diseases. 3 , 4 , 5 , 6 , 7 , 8 , 9 Emerging reports suggest that COVID‐19 may lead to autoimmune and autoinflammatory diseases, which in turn lead COVID‐19 patients to enter a vicious circle of infection and are closely associated with increased morbidity and mortality. 4 , 8 , 10 Among these studies, great attention has been focused on inflammatory bowel disease (IBD) which have a lot of overlap with COVID‐19 in clinical symptoms and immune activation patterns.…”

Section: Introductionmentioning

confidence: 99%

“…Severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) RNA can be detected in the stool examination of a large number of patients, suggesting that COVID‐19 may also invade the GI tract, which is the largest immune interface between the human body and the environment, constantly exposed to various antigens and potential immune stimuli 2 . Moreover, it has been found that in addition to complications during illness, COVID‐19 patients are often observed to experience late‐onset complications, including interstitial pneumonia, cytopenia, arthralgia, myocarditis, and autoimmune diseases 3–9 . Emerging reports suggest that COVID‐19 may lead to autoimmune and autoinflammatory diseases, which in turn lead COVID‐19 patients to enter a vicious circle of infection and are closely associated with increased morbidity and mortality 4,8,10 .…”

Section: Introductionmentioning

confidence: 99%

COVID‐19 and inflammatory bowel disease crosstalk: From emerging association to clinical proposal

Tao

Wang

Yang

et al. 2022

Journal of Medical Virology

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Severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) infection can cause coronavirus disease 2019 (COVID‐19), an acute respiratory inflammation that has emerged worldwide since December 2019, and it quickly became a global epidemic. Inflammatory bowel disease (IBD) is a group of chronic nonspecific intestinal inflammatory diseases whose etiology has not been elucidated. The two have many overlapping symptoms in clinical presentation, such as abdominal pain, diarrhea, pneumonia, etc. Imbalance of the autoimmune system in IBD patients and long‐term use of immunosuppressive drugs may increase the risk of infection; and systemic symptoms caused by COVID‐19 may also induce or exacerbate intestinal inflammation. It has been found that the SARS‐CoV‐2 receptor angiotensin converting enzyme 2, which is highly expressed in the lung and intestine, is an inflammatory protective factor, and is downregulated and upregulated in COVID‐19 and IBD, respectively, suggesting that there may be a coregulatory pathway. In addition, the immune activation pattern of COVID‐19 and the cytokine storm in the inflammatory response have similar roles in IBD, indicating that the two diseases may influence each other. Therefore, this review aimed to address the following research questions: whether SARS‐CoV‐2 infection leads to the progression of IBD; whether IBD increases the risk of COVID‐19 infection and poor prognosis; possible common mechanisms and genetic cross‐linking between the two diseases; new treatment and care strategies for IBD patients, and the feasibility and risk of vaccination in the context of the COVID‐19 epidemic.

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“…Therefore, an effective animal model is useful for coronavirus-related immune injury research. In particular, an increasing number of autoimmune diseases related to COVID-19 infection have been reported recently, which has drawn more attention to the immune system damage caused by the imbalance of inflammatory factors after SARS-CoV-2 infection (4,5). Previous reports of multiple cases of immune system damage after COVID-19 have revealed that very little is known about the complexity of COVID-19, and a reliable animal model of coronavirusassociated immune damage is necessary to support related research.…”

Section: Introductionmentioning

confidence: 99%

Potential mouse models of coronavirus-related immune injury

Nan

Wu²,

Su³

et al. 2022

Front. Immunol.

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Basic research for prevention and treatment of coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), continues worldwide. In particular, multiple newly reported cases of autoimmune-related diseases after COVID-19 require further research on coronavirus-related immune injury. However, owing to the strong infectivity of SARS-CoV-2 and the high mortality rate, it is difficult to perform relevant research in humans. Here, we reviewed animal models, specifically mice with coronavirus-related immune disorders and immune damage, considering aspects of coronavirus replacement, viral modification, spike protein, and gene fragments. The evaluation of mouse models of coronavirus-related immune injury may help establish a standardised animal model that could be employed in various areas of research, such as disease occurrence and development processes, vaccine effectiveness assessment, and treatments for coronavirus-related immune disorders. COVID-19 is a complex disease and animal models cannot comprehensively summarise the disease process. The application of genetic technology may change this status.

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Multisystem Inflammatory Syndrome and Autoimmune Diseases Following COVID-19: Molecular Mechanisms and Therapeutic Opportunities

Cited by 26 publications

References 214 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?

COVID‐19 and inflammatory bowel disease crosstalk: From emerging association to clinical proposal

Potential mouse models of coronavirus-related immune injury

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