Type I IFNs and CD8 T cells increase intestinal barrier permeability after chronic viral infection.

ABSTRACT: Intestinal barrier leakage constitutes a potential therapeutic target for many inflammatory diseases and represents a disease progression marker during chronic viral infections. However, the causes of altered gut barrier remain mostly unknown. Using murine infection with lymphocytic choriomeningitis virus, we demonstrate that, in contrast to an acute viral strain, a persistent viral isolate leads to long-term viral replication in hematopoietic and mesenchymal cells, but not epithelial cells (IECs), in the intestine. Viral persistence drove sustained intestinal epithelial barrier leakage, which was characterized by increased paracellular flux of small molecules and was associated with enhanced colitis susceptibility. Type I IFN signaling caused tight junction dysregulation in IECs, promoted

SUBMITTER: Labarta-Bajo L 

PROVIDER: S-EPMC7953738 | biostudies-literature | 2020 Dec

REPOSITORIES: biostudies-literature