https://ogma.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:47737 Wed 25 Jan 2023 15:07:49 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:25787 Wed 11 Apr 2018 16:15:49 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:14773 Wed 11 Apr 2018 11:04:31 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:11796 Wed 11 Apr 2018 10:08:46 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:39240 h2 signalling, improved their outcomes. Methods: Male BALB/c mice were intranasally sensitized with house dust mite antigen (Der p 1) for 2 weeks; the mice were then inoculated intranasally with a single dose of pandemic H1N1 (pH1N1). The mice were administered intraperitoneally anti-IL-4Rα through either a prophylactic or a therapeutic treatment strategy. Results: Infection with pH1N1 of mice sensitized to house dust mite (HDM) led to a 24% loss in weight by day 7 of infection (versus 14% in non-sensitized mice; p < .05). This was accompanied by increased viral load in the airways and a dampened anti-viral host responses to the infection. Treatment of HDM sensitized mice with a monoclonal antibody against IL-4Rα prior to or following pH1N1 infection prevented the excess weight loss, reduced the viral load in the lungs and ameliorated airway eosinophilia and systemic inflammation related to the pH1N1 infection. Conclusion: Together, these data implicate allergic asthma as a significant risk factor for H1N1-related morbidity and reveal a potential therapeutic role for IL-4Rα signalling blockade in reducing the severity of influenza infection in those with allergic airway disease.]]> Wed 10 Aug 2022 08:53:16 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:53281 Tue 21 Nov 2023 10:18:02 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:48952 Tue 02 May 2023 11:43:55 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:36808 Thu 04 Nov 2021 10:39:56 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:16017 Sat 24 Mar 2018 08:19:30 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:11486 Sat 24 Mar 2018 08:10:26 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:19878 Sat 24 Mar 2018 07:57:00 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:26099 TM Western assays. Transepithelial permeability assays were performed to assess effects on barrier functionality. RT2 Profiler focused qPCR arrays and pathway analysis evaluating associations between human TJ and antiviral response were performed to identify potential interactions and pathways between genes of interests. Results: HRV-1B infection affected viability that was both time and TCID⁵⁰ dependent. Significant increases in apoptosis and viral replication post-infection correlated with viral titer. Viral infection significantly decreased claudin-1 protein expression at the lower TCID⁵⁰, while a significant decrease in all three TJ protein expressions occurred at higher TCID⁵⁰. Decrease in protein expression was concomitant with significant increases in epithelial permeability of fluorescein isothiocynate labeled-dextran 4 and 20 kDa. Analysis of focused qPCR arrays demonstrated a significant decrease in ZO-1 gene expression. Furthermore, network analysis between human TJ and antiviral response genes revealed possible interactions and regulation of TJ genes via interleukin (IL)-15 in response to HRV-1B infection. Conclusion: HRV-1B infection directly alters human airway epithelial TJ expression leading to increased epithelial permeability potentially via an antiviral response of IL-15.]]> Sat 24 Mar 2018 07:39:52 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:46061 in vitro in human airway epithelial cell cultures and in vivo in mouse models of ICS administration. Mice deficient in the type I IFN-α/β receptor (Ifnar1^-/-) and administration of exogenous IFN-β were used to study the functional role of type-I interferon signaling in ACE2 expression. We compared sputum ACE2 expression in patients with COPD stratified according to use or nonuse of ICS. Results: ICS administration attenuated ACE2 expression in mice, an effect that was reversed by exogenous IFN-β administration, and Ifnar1^-/- mice had reduced ACE2 expression, indicating that type I interferon contributes mechanistically to this effect. ICS administration attenuated expression of ACE2 in airway epithelial cell cultures from patients with COPD and in mice with elastase-induced COPD-like changes. Compared with ICS nonusers, patients with COPD who were taking ICSs also had reduced sputum expression of ACE2. Conclusion: ICS therapies in COPD reduce expression of the SARS-CoV-2 entry receptor ACE2. This effect may thus contribute to altered susceptibility to COVID-19 in patients with COPD.]]> Fri 11 Nov 2022 14:22:05 AEDT ]]>