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Receptor for advanced glycation end-products axis and coronavirus disease 2019 in inflammatory bowel diseases: A
Armando Rojas1, Iván Schneider2, Cristian Lindner2
1Biomedical Research Labs, Medicine Faculty, Catholic University of Maule, Talca 3634000, Chile. arojasr@ucm.cl.
Abstract:
Compelling evidence supports the crucial role of the receptor for advanced glycation end-products (RAGE) axis activation in many clinical entities. Since the beginning of the coronavirus disease 2019 pandemic, there is an increasing concern about the risk and handling of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection in inflammatory gastrointestinal disorders, such as inflammatory bowel diseases (IBD). However, clinical data raised during pandemic suggests that IBD patients do not have an increased risk of contracting SARS-CoV-2 infection or develop a more severe course of infection. In the present review, we intend to highlight how two potentially important contributors to the inflammatory response to SARS-CoV-2 infection in IBD patients, the RAGE axis activation as well as the cross-talk with the renin-angiotensin system, are dampened by the high expression of soluble forms of both RAGE and the angiotensin-converting enzyme (ACE) 2. The soluble form of RAGE functions as a decoy for its ligands, and soluble ACE2 seems to be an additionally attenuating contributor to RAGE axis activation, particularly by avoiding the transactivation of the RAGE axis that can be produced by the virus-mediated imbalance of the ACE/angiotensin II/angiotensin II receptor type 1 pathway.
Insights
Inflammatory bowel disease (IBD) patients show dampened responses to SARS-CoV-2 infection due to high levels of soluble RAGE and ACE2. These soluble factors act as decoys, mitigating severe inflammatory pathways.
Area of Science:
- Immunology
- Gastroenterology
- Virology
Background:
- The receptor for advanced glycation end-products (RAGE) axis is implicated in various clinical conditions.
- Concerns arose regarding SARS-CoV-2 infection risk and severity in inflammatory bowel disease (IBD) patients.
- Emerging data indicate IBD patients do not face increased SARS-CoV-2 infection risk or severity.
Purpose of the Study:
- To explore the mechanisms dampening SARS-CoV-2 inflammatory responses in IBD patients.
- To investigate the roles of RAGE axis activation and its cross-talk with the renin-angiotensin system.
- To highlight the impact of soluble RAGE and soluble ACE2 in mitigating these inflammatory pathways.
Main Methods:
- Review of existing clinical data and scientific literature.
- Analysis of the interplay between RAGE, SARS-CoV-2, and the renin-angiotensin system.
- Focus on the modulatory effects of soluble RAGE and soluble ACE2.
Main Results:
- IBD patients exhibit high expression of soluble RAGE and soluble ACE2.
- Soluble RAGE acts as a decoy, binding to RAGE ligands and reducing axis activation.
- Soluble ACE2 further attenuates RAGE axis activation, particularly during SARS-CoV-2 infection.
Conclusions:
- High levels of soluble RAGE and soluble ACE2 in IBD patients mitigate inflammatory responses to SARS-CoV-2.
- These soluble factors protect against excessive RAGE axis activation and associated pathology.
- The findings offer insights into the specific inflammatory profiles of IBD patients during viral infections.
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