5. Conclusion
Our data propose that SARS-CoV-2 disrupts pathways associated with innate immune responses and GI barrier function, leading to intestinal low-grade inflammation and mucosal barrier leakage. We identified pre-existing GI complaints as a risk factor for developing PCS Fatigue. Specific immune phenotypes, particularly in the innate immune response, appear to be critical in regulating GI barrier integrity. Our data indicate that PCS patients exhibit a higher LBP/sCD14 ratio, lower IL-33 levels and higher IL-6 levels compared to the control groups, suggesting an intestinal leakage and subsequent low-grade inflammation. Medical record data of our study cohort shows that GI complaints, but also susceptibility to infections and signs of hypermobility were already present before SARS-CoV-2 infection, in contrast to fully convalescent participants.
Overall, our study highlights the critical role of the GI tract in PCS Fatigue development. Monitoring GI symptoms and markers not only during and after an acute SARS-CoV-2 infection, but also as baseline records is needed for identifying predictive clinical phenotypes for PCS. Understanding the interplay between viral infections, immune responses, and gut integrity could lead to more effective diagnostic and treatment approaches, alleviating the burden on affected individuals and healthcare systems.
Tables
Table 1: Demographics, information on the COVID-19 disease course and vaccination state of the study cohort.