COVID-19 as a potential trigger for ulcerative colitis

Abstract

SARS-CoV-2 infection is a global pathology. Recent international studies have reported involvement of various organs, including the gastrointestinal system. It was shown that incidence rates of inflammatory bowel diseases (IBD) such as Crohn’s disease and ulcerative colitis (UC) were 14.6% and 10% higher during the pandemic respectively than rates during the pre-COVID-19 period. Also, COVID-19 has been found to increase the risk of developing new autoimmune diseases. Materials and methods: The study included scientific publications, selected by keywords in the database PubMed, Google Scholar, and Hinari. Results: The angiotensin-converting enzyme receptor (ACE2) is highly expressed in the terminal ileum and colon. The surface receptor ACE2 interacts directly with the spike glycoprotein (protein S), which allows the virus to enter cells and reproduce new virions, followed by its replication and the initiation of an advanced inflammatory process. SARS-CoV-2 can result in alteration of gut microbiota and increased risk of intestinal inflammation. COVID-19 moderately severe form is characterized by a cytokine storm in which there are extensive neutrophils, lymphocytes, macrophages and immune mediators, including tumor necrosis factor (TNF), the major inflammatory mediator in IBD and in almost all acute inflammatory reactions. Conclusions: The latest research has provided evidence about the ability of infections to precipitate autoimmune diseases. In this case, the causative organism is not necessarily isolated from gastrointestinal cells, and the enhanced inflammatory response after infection can eliminate the infectious agent. However, in people genetically sensitive to IBD, the initial immune reaction can turn into a chronic response, leading to disease.