https://nova.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 miR-122 promotes virus-induced lung disease by targeting SOCS1 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:45152 Wed 26 Oct 2022 13:51:48 AEDT ]]> Modeling of respiratory syncytial virus-induced exacerbation of allergic airways disease https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:27889 Wed 11 Apr 2018 14:53:06 AEST ]]> Bromodomain and extra terminal (BET) inhibitor suppresses macrophage-driven steroid-resistant exacerbations of airway hyper-responsiveness and inflammation https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:30136 Wed 10 Nov 2021 15:14:29 AEDT ]]> Potential Role of MicroRNAs in the Regulation of Antiviral Responses to influenza infection https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:43373 Thu 15 Sep 2022 15:46:34 AEST ]]> A critical role for the CXCL3/CXCL5/CXCR2 neutrophilic chemotactic axis in the regulation of type 2 responses in a model of rhinoviral-induced asthma exacerbation https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:40298 Thu 11 May 2023 14:03:27 AEST ]]> TNF-α and macrophages are critical for respiratory syncytial virus-induced exacerbations in a mouse model of allergic airways disease https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:24758 Sat 24 Mar 2018 07:14:04 AEDT ]]> Identification of IFN-γ and IL-27 as critical regulators of respiratory syncytial virus-induced exacerbation of allergic airways disease in a mouse model https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:33087 Fri 24 Aug 2018 16:25:53 AEST ]]> MicroRNA-21 drives severe, steroid-insensitive experimental asthma by amplifying phosphoinositide 3-kinase-mediated suppression of histone deacetylase 2 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:33077 Chlamydia, Haemophilus influenzae, influenza, and respiratory syncytial virus respiratory tract infections and ovalbumin-induced, severe, steroid-insensitive allergic airway disease (SSIAAD) in BALB/c mice were developed and interrogated. Results: Infection induced increases in the levels of microRNA (miRNA)-21 (miR-21) expression in the lung during SSIAAD, whereas expression of the miR-21 target phosphatase and tensin homolog was reduced. This was associated with an increase in levels of phosphorylated Akt, an indicator of phosphoinositide 3-kinase (PI3K) activity, and decreased nuclear histone deacetylase (HDAC)2 levels. Treatment with an miR-21-specific antagomir (Ant-21) increased phosphatase and tensin homolog levels. Treatment with Ant-21, or the pan-PI3K inhibitor LY294002, reduced PI3K activity and restored HDAC2 levels. This led to suppression of airway hyperresponsiveness and restored steroid sensitivity to allergic airway disease. These observations were replicated with SSIAAD associated with 4 different pathogens. Conclusion: We identify a previously unrecognized role for an miR-21/PI3K/HDAC2 axis in SSIAAD. Our data highlight miR-21 as a novel therapeutic target for the treatment of this form of asthma.]]> Fri 24 Aug 2018 14:41:05 AEST ]]> IL-17A is a common and critical driver of impaired lung function and immunopathology induced by influenza virus, rhinovirus and respiratory syncytial virus https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:49776 Fri 02 Jun 2023 17:29:57 AEST ]]>