https://ogma.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 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:33143 −26) and a 1.4 fold in the severe COPD -related genes (P = 2.3 × 10⁻¹²). There was no significant enrichment of the mice and human smoking-related genes in mild COPD signature. These data suggest that murine smoke models are strongly representative of molecular processes of human smoking but less of COPD.]]> Tue 03 Sep 2019 18:18:55 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:16915 10) activates the nucleotide-binding domain, leucine-rich repeat protein (NLRP) 3 inflammasome in human airway epithelial cells. Our objective was to determine the innate and adaptive immune responses mediated by the airway epithelium NLRP3 inflammasome in response to PM₁₀ exposure. Using in vitro cultures of human airway epithelial cells and in vivo studies with wild-type and Nlrp3^-/- mice, we investigated the downstream consequences of PM₁₀-induced NLPR3 inflammasome activation on cytokine production, cellular inflammation, dendritic cell activation, and PM₁₀-facilitated allergic sensitization. PM₁₀ activates an NLRP3 inflammasome/IL-1 receptor I (IL-1RI) axis in airway epithelial cells, resulting in IL-1β, CC chemokine ligand-20, and granulocyte/macrophage colony–stimulating factor production, which is associated with dendritic cell activation and lung neutrophilia. Despite these profound innate immune responses in the airway epithelium, the NLRP3 inflammasome/IL-1RI axis is dispensable for PM₁₀-facilitated allergic sensitization. We demonstrate the importance of the lung NLRP3 inflammasome in mediating PM₁₀ exposure–associated innate, but not adaptive, immune responses. Our study highlights a mechanism by which PM₁₀ exposure can contribute to the exacerbation of airway disease, but not PM₁₀-facilitated allergic sensitization.]]> Sat 24 Mar 2018 07:58:45 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:19679 Sat 24 Mar 2018 07:53:38 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:23803 Sat 24 Mar 2018 07:12:53 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:46962 Il22^−/−) mice. CS-induced airway remodelling and emphysema-like alveolar enlargement did not occur in Il22^−/− mice. Il22^−/− mice had improved lung function in terms of airway resistance, total lung capacity, inspiratory capacity, forced vital capacity and compliance. These data highlight important roles for IL-22 and its receptors in human COPD and CS-induced experimental COPD.]]> Mon 12 Dec 2022 14:27:30 AEDT ]]>