https://nova.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:50653 Wed 28 Feb 2024 15:55:38 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:51924 Wed 28 Feb 2024 09:57:50 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:52146 Wed 04 Oct 2023 10:20:41 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:49742 Tue 30 May 2023 15:22:46 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:47290 Tue 30 Apr 2024 08:50:07 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:47798 Tue 28 Mar 2023 15:16:40 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:37877 Thu 28 Oct 2021 13:02:25 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:38305 Thu 26 Aug 2021 11:11:37 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:36808 Thu 04 Nov 2021 10:39:56 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:34569 Thu 04 Nov 2021 10:38:24 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:46830 Thu 01 Dec 2022 11:45:24 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:35652 Mon 20 Nov 2023 11:12:20 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:35650 Mon 13 Nov 2023 11:04:35 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:36049 Fri 31 Jan 2020 13:13:08 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:55346 Fri 17 May 2024 15:50:21 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:41554 Fri 05 Aug 2022 14:23:21 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:36769 Fri 03 Jul 2020 14:34:42 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:33480 -/-) BALB/c mice were infected intranasally with RV1B. In separate experiments, Tnfsf10^-/- mice were sensitized and challenged via the airway route with house dust mite (HDM) to induce allergic airways disease and then challenged with RVIB or UV-RVIB. Airway hyperreactivity (AHR) was invasively assessed as total airways resistance in response to increasing methacholine challenge and inflammation was assessed in bronchoalveolar lavage fluid at multiple time points postinfection. Chemokines were quantified by ELISA of whole lung lysates and viral load was determined by quantitative RT-PCR and tissue culture infective dose (TCID₅₀). Human airway epithelial cells (BEAS2B) were infected with RV1B and stimulated with recombinant TRAIL or neutralizing anti-TRAIL antibodies and viral titer assessed by TCID₅₀. HDM-challenged Tnfsf10 ^-/- mice were protected against RV-induced AHR and had suppressed cellular infiltration in the airways upon RV infection. Chemokine C-X-C-motif ligand 2 (CXCL2) production was suppressed in naïve Tnfsf10^-/- mice infected with RV1B, with less RV1B detected 24 h postinfection. This was associated with reduced apoptotic cell death and a reduction of interferon (IFN)-λ2/3 but not IFN-α or IFN-β. TRAIL stimulation increased, whereas anti-TRAIL antibodies reduced viral replication in RV1B-infected BEAS2B cells in vitro. In conclusion, TRAIL promotes RV-induced AHR, inflammation and RV1B replication, implicating this molecule and its downstream signaling pathways as a possible target for the amelioration of RV1B-induced allergic and nonallergic lung inflammation and AHR.]]> Fri 01 Apr 2022 09:25:03 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:33085 -/-) and TLR4-deficient (Tlr4^-/-) mice. CS-induced airway fibrosis, characterized by increased collagen deposition around small airways, was not altered in Tlr2^-/- mice but was attenuated in Tlr4^-/- mice compared with CS-exposed WT controls. However, Tlr2^-/- mice had increased CS-induced emphysema-like alveolar enlargement, apoptosis, and impaired lung function, while these features were reduced in Tlr4^-/- mice compared with CS-exposed WT controls. Taken together, these data highlight the complex roles of TLRs in the pathogenesis of COPD and suggest that activation of TLR2 and/or inhibition of TLR4 may be novel therapeutic strategies for the treatment of COPD.]]> Fri 01 Apr 2022 09:24:33 AEDT ]]>