tetano
Editor, Senior Moderator
J Histochem Cytochem
. 2021 Oct 19;221554211054447.
doi: 10.1369/00221554211054447. Online ahead of print.
Type I Interferon Signaling Increases Versican Expression and Synthesis in Lung Stromal Cells During Influenza Infection
Jourdan E Brune[SUP] 1 2 [/SUP], Mary Y Chang[SUP] 1 2 [/SUP], William A Altemeier[SUP] 1 3 [/SUP], Charles W Frevert[SUP] 1 2 3 [/SUP]
Affiliations
Abstract
Versican, a chondroitin sulfate proteoglycan, is an essential component of the extracellular matrix (ECM) in inflammatory lung disease. Versican's potential as an immunomodulatory molecule makes it a promising therapeutic target for controlling host immune responses in the lungs. To establish changes to versican expression and accumulation during influenza A viral pneumonia, we document the temporal and spatial changes to versican mRNA and protein in concert with pulmonary inflammatory cell infiltration. These studies were performed in the lungs of wild-type C57BL6/J mice on days 3, 6, 9, and 12 post-infection with influenza A virus using immunohistochemistry, in situ hybridization, and quantitative digital pathology. Using duplex in situ hybridization, we demonstrate that type I interferon signaling contributes significantly to versican expression in lung stromal cells. Our findings show that versican is a type I interferon-stimulated gene in pulmonary fibroblasts and pericytes in the context of viral pneumonia. These data also provide a guide for future studies to determine the role of versican in the pulmonary immune response to influenza infection.
Keywords: artificial intelligence; fibroblasts; myeloid cells; pericytes; quantitative digital pathology.
. 2021 Oct 19;221554211054447.
doi: 10.1369/00221554211054447. Online ahead of print.
Type I Interferon Signaling Increases Versican Expression and Synthesis in Lung Stromal Cells During Influenza Infection
Jourdan E Brune[SUP] 1 2 [/SUP], Mary Y Chang[SUP] 1 2 [/SUP], William A Altemeier[SUP] 1 3 [/SUP], Charles W Frevert[SUP] 1 2 3 [/SUP]
Affiliations
- PMID: 34666527
- DOI: 10.1369/00221554211054447
Abstract
Versican, a chondroitin sulfate proteoglycan, is an essential component of the extracellular matrix (ECM) in inflammatory lung disease. Versican's potential as an immunomodulatory molecule makes it a promising therapeutic target for controlling host immune responses in the lungs. To establish changes to versican expression and accumulation during influenza A viral pneumonia, we document the temporal and spatial changes to versican mRNA and protein in concert with pulmonary inflammatory cell infiltration. These studies were performed in the lungs of wild-type C57BL6/J mice on days 3, 6, 9, and 12 post-infection with influenza A virus using immunohistochemistry, in situ hybridization, and quantitative digital pathology. Using duplex in situ hybridization, we demonstrate that type I interferon signaling contributes significantly to versican expression in lung stromal cells. Our findings show that versican is a type I interferon-stimulated gene in pulmonary fibroblasts and pericytes in the context of viral pneumonia. These data also provide a guide for future studies to determine the role of versican in the pulmonary immune response to influenza infection.
Keywords: artificial intelligence; fibroblasts; myeloid cells; pericytes; quantitative digital pathology.