https://nova.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:22168 -/-) BALB/c mice were intranasally sensitised and challenged with HDM prior to infection with RV1B. In some experiments, mice were administered recombinant IFN or adoptively transferred with plasmacytoid dendritic cells (pDC). Results: Allergic Tlr7^-/- mice displayed impaired IFN release upon RV1B infection, increased virus replication and exaggerated eosinophilic inflammation and airways hyper reactivity. Treatment with exogenous IFN or adoptive transfer of TLR7-competent pDCs blocked these exaggerated inflammatory responses and boosted IFNγ release in the absence of host TLR7 signalling. TLR7 expression in the lungs was suppressed by allergic inflammation and by interleukin (IL)-5-induced eosinophilia in the absence of allergy. Subjects with moderate-to-severe asthma and eosinophilic but not neutrophilic airways inflammation, despite inhaled steroids, showed reduced TLR7 and IFNλ2/3 expression in endobronchial biopsies. Furthermore, TLR7 expression inversely correlated with percentage of sputum eosinophils. Conclusions: This implicates IL-5-induced airways eosinophilia as a negative regulator of TLR7 expression and antiviral responses, which provides a molecular mechanism underpinning the effect of eosinophil-targeting treatments for the prevention of asthma exacerbations.]]> Wed 11 Apr 2018 15:36:21 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:17053 Wed 11 Apr 2018 15:00:47 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:28036 Wed 11 Apr 2018 12:47:04 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:27569 Wed 11 Apr 2018 11:56:33 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:15055 Wed 11 Apr 2018 09:51:04 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:32190 Wed 09 Mar 2022 16:01:03 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:54610 Wed 06 Mar 2024 10:38:44 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:49079 Wed 03 May 2023 16:14:55 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:46337 P = .01), emergency visit (RR = 8.61, P = .03), and hospitalization (RR = 12.94, P < .01). Results of the cluster analysis were successfully validated in an independent PGA population classified using decision tree analysis. Although PGA can transform into or develop from other phenotypes, 70% were stable over time. Conclusions: Among 3 identified PGA clusters, cluster 3 had a higher risk of severe exacerbation. PGA heterogeneity indicates the requirement of novel targeted interventions.]]> Tue 15 Nov 2022 15:03:45 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:47009 Tue 13 Dec 2022 11:34:29 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:38811 Tue 08 Feb 2022 14:30:33 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:51880 Thu 21 Sep 2023 10:25:03 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:54912 Thu 21 Mar 2024 12:03:37 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:19655 Sat 24 Mar 2018 08:01:13 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:16920 Sat 24 Mar 2018 08:00:29 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:18986 20% occurred in only one subject with AECOPD who was in GOLD category III. The decrease in percentage of FEV1 from baseline was greatest in the second stage of induction, and correlated with that of the final stage (r = 0.589; P = 0.01). The fall in FEV1 during induction increased with GOLD category (P < 0.05). Conclusions:  SI can be safely and successfully performed in patients with moderate to very severe chronic obstructive pulmonary disease who experience an exacerbation using this modified induction protocol. The early decrease in FEV1 can be used to predict the maximum fall.]]> Sat 24 Mar 2018 07:58:51 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:5000 Sat 24 Mar 2018 07:44:09 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:41841 Tnfsf10^−/− BALB/c mice were administered bleomycin to induce fibrosis and some groups were treated with the FTY720 analogue AAL(s) to activate PP2A. Mouse fibroblasts were treated with recombinant TRAIL and fibrotic responses were assessed. Results: TRAIL in serum and MID1 protein levels in biopsies from IPF patients were increased compared to controls. MID1 levels were inversely associated while PP2A activity levels correlated with DLco. Tnfsf10^−/− and mice treated with the PP2A activator AAL(s) were largely protected against bleomycin-induced reductions in lung function and fibrotic changes. Addition of recombinant TRAIL to mouse fibroblasts in-vitro increased collagen production which was reversed by PP2A activation with AAL(s). Conclusion: TRAIL signalling through MID1 deactivates PP2A and promotes fibrosis with corresponding lung function decline. This may provide novel therapeutic targets for IPF.]]> Mon 15 Aug 2022 10:15:38 AEST ]]>