IL-17RA promotes pathologic epithelial inflammation in a mouse model of upper respiratory influenza infection.
Ontology highlight
ABSTRACT: The upper respiratory tract (nasopharynx or NP) is the first site of influenza replication, allowing the virus to disseminate to the lower respiratory tract or promoting community transmission. The host response in the NP regulates an intricate balance between viral control and tissue pathology. The hyper-inflammatory responses promote epithelial injury, allowing for increased viral dissemination and susceptibility to secondary bacterial infections. However, the pathologic contributors to influenza upper respiratory tissue pathology are incompletely understood. In this study, we investigated the role of interleukin IL-17 recetor A (IL-17RA) as a modulator of influenza host response and inflammation in the upper respiratory tract. We used a combined experimental approach involving IL-17RA-/
SUBMITTER: Navaeiseddighi Z
PROVIDER: S-EPMC10729944 | biostudies-literature | 2023 Dec
REPOSITORIES: biostudies-literature
ACCESS DATA