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- W2156830712 abstract "ABSTRACT Rhinoviral infection is an important trigger of acute inflammatory exacerbations in patients with underlying airway disease. We have previously established that interleukin-1β (IL-1β) is central in the communication between epithelial cells and monocytes during the initiation of inflammation. In this study we explored the roles of IL-1β and its signaling pathways in the responses of airway cells to rhinovirus-1B (RV-1B) and further determined how responses to RV-1B were modified in a model of bacterial coinfection. Our results revealed that IL-1β dramatically potentiated RV-1B-induced proinflammatory responses, and while monocytes did not directly amplify responses to RV-1B alone, they played an important role in the responses observed with our coinfection model. MyD88 is the essential signaling adapter for IL-1β and most Toll-like receptors. To examine the role of MyD88 in more detail, we created stable MyD88 knockdown epithelial cells using short hairpin RNA (shRNA) targeted to MyD88. We determined that IL-1β/MyD88 plays a role in regulating RV-1B replication and the inflammatory response to viral infection of airway cells. These results identify central roles for IL-1β and its signaling pathways in the production of CXCL8, a potent neutrophil chemoattractant, in viral infection. Thus, IL-1β is a viable target for controlling the neutrophilia that is often found in inflammatory airway disease and is exacerbated by viral infection of the airways." @default.
- W2156830712 created "2016-06-24" @default.
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- W2156830712 date "2011-08-01" @default.
- W2156830712 modified "2023-09-25" @default.
- W2156830712 title "Role of Interleukin-1 and MyD88-Dependent Signaling in Rhinovirus Infection" @default.
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- W2156830712 doi "https://doi.org/10.1128/jvi.02649-10" @default.
- W2156830712 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3147909" @default.
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