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.