| Autor: |
Bruland T; Department of Clinical and Molecular Medicine, Norwegian University of Science and Technology, 7491 Trondheim, Norway.; Department of Gastroenterology and Hepatology, Clinic of Medicine, St. Olav's University Hospital, 7030 Trondheim, Norway., Østvik AE; Department of Clinical and Molecular Medicine, Norwegian University of Science and Technology, 7491 Trondheim, Norway.; Department of Gastroenterology and Hepatology, Clinic of Medicine, St. Olav's University Hospital, 7030 Trondheim, Norway., Sandvik AK; Department of Clinical and Molecular Medicine, Norwegian University of Science and Technology, 7491 Trondheim, Norway.; Department of Gastroenterology and Hepatology, Clinic of Medicine, St. Olav's University Hospital, 7030 Trondheim, Norway.; Centre of Molecular Inflammation Research, Norwegian University of Science and Technology, 7491 Trondheim, Norway., Hansen MD; Department of Clinical and Molecular Medicine, Norwegian University of Science and Technology, 7491 Trondheim, Norway.; Department of Medical Microbiology, Clinic of Laboratory Medicine, St. Olav's University Hospital, 7030 Trondheim, Norway. |
| Abstrakt: |
Ulcerative colitis is characterized by relapsing and remitting colonic mucosal inflammation. During the early stages of viral infection, innate immune defenses are activated, leading to the rapid release of cytokines and the subsequent initiation of downstream responses including inflammation. Previously, intestinal viruses were thought to be either detrimental or neutral to the host. However, persisting viruses may have a role as resident commensals and confer protective immunity during inflammation. On the other hand, the dysregulation of gut mucosal immune responses to viruses can trigger excessive, pathogenic inflammation. The purpose of this review is to discuss virus-induced innate immune responses that are at play in ulcerative colitis. |
