https://ogma.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:50469 Wed 28 Feb 2024 15:49:48 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:50453 Wed 28 Feb 2024 15:13:31 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:21992 Bacillus species were identified compared with healthy controls. PCR analyses revealed increased rates of detection of potentially pathogenic bacteria with Haemophilus influenzae detection associated with higher sputum levels of NE and IL-1β, while Streptococcus pneumoniae was more common in male ex-smokers with emphysema and a deficit in diffusion capacity. Conclusion: Non-pathogenic and pathogenic bacteria were altered in the sputum of patients with COPD. These observations highlight the potential to identify treatment and management strategies that both target specific bacterial pathogens and restore the microbial balance, which may lead to reductions in inflammation and subsequent improvements in lung health.]]> Wed 17 Nov 2021 16:31:05 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:41157 Wed 15 Feb 2023 10:57:18 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:47060 Wed 13 Mar 2024 08:04:20 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:41553 Wed 08 May 2024 09:45:18 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:49760 Tue 30 May 2023 18:39:10 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:47013 Tue 13 Dec 2022 11:48:24 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:47003 Tue 13 Dec 2022 10:59:30 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:33793 –/–) mice had reduced mucin (MUC) 5 AC levels, but not MUC5B levels, in the airways as compared with wild‐type (WT) mice. Fbln1c interacted with fibronectin and periostin that was linked to collagen deposition around the small airways. Fbln1c^–/– mice with AAD also had reduced numbers of α‐smooth muscle actin‐positive cells around the airways and reduced airway contractility as compared with WT mice. After HDM challenge, these mice also had fewer airway inflammatory cells, reduced interleukin (IL)‐5, IL‐13, IL‐33, tumour necrosis factor (TNF) and CXCL1 levels in the lungs, and reduced IL‐5, IL‐33 and TNF levels in lung‐draining lymph nodes. Therapeutic targeting of Fbln1c reduced the numbers of GATA3‐positive Th2 cells in the lymph nodes and lungs after chronic HDM challenge. Treatment also reduced the secretion of IL‐5 and IL‐13 from co‐cultured dendritic cells and T cells restimulated with HDM extract. Human epithelial cells cultured with Fbln1c peptide produced more CXCL1 mRNA than medium‐treated controls. Our data show that Fbln1c may be a therapeutic target in chronic asthma.]]> Thu 28 Oct 2021 13:02:39 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:41158 Thu 28 Jul 2022 09:27:19 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:45342 Thu 27 Oct 2022 15:17:41 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:45318 Thu 27 Oct 2022 13:56:46 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:47210 Thu 15 Dec 2022 17:18:38 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:15999 Sat 24 Mar 2018 08:19:32 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:21997 Sat 24 Mar 2018 07:14:33 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:42355 Mon 22 Aug 2022 14:01:30 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:53538 Mon 04 Dec 2023 15:44:36 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:42107 Fri 26 Aug 2022 11:23:51 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:48427 Fri 26 Apr 2024 13:31:04 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:33076 Chlamydia and Haemophilus respiratory infection-mediated, ovalbumin-induced severe, steroid-resistant allergic airway disease. These models share the hallmark features of human disease, including elevated airway neutrophils, and NLRP3 inflammasome and IL-1ß responses. The roles and potential for targeting of NLRP3 inflammasome, caspase-1, and IL-1ß responses in experimental severe, steroid-resistant asthma were examined using a highly selective NLRP3 inhibitor, MCC950; the specific caspase-1 inhibitor Ac-YVAD-cho; and neutralizing anti-IL-1ß antibody. Roles for IL-1ß-induced neutrophilic inflammation were examined using IL-1ß and anti-Ly6G. Measurements and Main Results: Chlamydia and Haemophilus infections increase NLRP3, caspase-1, IL-1ß responses that drive steroid-resistant neutrophilic inflammation and airway hyperresponsiveness. Neutrophilic airway inflammation, disease severity, and steroid resistance in human asthma correlate with NLRP3 and IL-1ß expression. Treatment with anti-IL-1ß, Ac- YVAD-cho, and MCC950 suppressed IL-1ß responses and the important steroid-resistant features of disease in mice, whereas IL-1ß administration recapitulated these features. Neutrophil depletion suppressed IL-1ß-induced steroid-resistant airway hyperresponsiveness. Conclusions: NLRP3 inflammasome responses drive experimental severe, steroid-resistant asthma and are potential therapeutic targets in this disease.]]> Fri 24 Aug 2018 14:40:56 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:40169 in vitro model of the pulmonary epithelial-endothelial barrier and novel murine models to investigate the role of glycemic variability in influenza severity. In vitro, a history of glycemic variability significantly increased influenza-driven cell death and destruction of the epithelial-endothelial barrier. In vivo, influenza virus-infected mice with a history of glycemic variability lost significantly more body weight than mice with constant blood glucose levels. This increased disease severity was associated with markers of oxidative stress and hyperinflammation both in vitr and in vivo. Together, these results provide the first indication that glycemic variability may help drive the increased risk of severe influenza in people with diabetes mellitus.]]> Fri 15 Jul 2022 10:39:14 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:55056 Fri 05 Apr 2024 14:28:53 AEDT ]]>