https://nova.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:50469 Wed 28 Feb 2024 15:49:48 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:52688 Wed 28 Feb 2024 15:49:25 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:45172 Wed 26 Oct 2022 14:18:41 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:26482 Wed 11 Apr 2018 15:59:51 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:12899 Wed 11 Apr 2018 15:23:55 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:28066 Klebsiella pneumoniae infection, cecal ligation and puncture as well as rhinovirus exacerbated asthma models were also assessed using PXS-4728A. Results: Selective VAP-1/SSAO inhibition by PXS-4728A diminished leukocyte rolling and adherence induced by CXCL1/KC. Inhibition of VAP-1/SSAO also dampened the migration of neutrophils to the lungs in response to LPS, Klebsiella pneumoniae lung infection and CLP induced sepsis; whilst still allowing for normal neutrophil defense function, resulting in increased survival. The functional effects of this inhibition were demonstrated in the RV exacerbated asthma model, with a reduction in cellular infiltrate correlating with a reduction in airways hyperractivity. Conclusions and implications: This study demonstrates that the endothelial cell ligand VAP-1/SSAO contributes to the migration of neutrophils during acute lung inflammation, pulmonary infection and airway hyperractivity. These results highlight the potential of inhibiting of VAP-1/SSAO enzymatic function, by PXS-4728A, as a novel therapeutic approach in lung diseases that are characterized by neutrophilic pattern of inflammation.]]> Wed 11 Apr 2018 14:12:30 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:10124 Wed 11 Apr 2018 10:19:59 AEST ]]> https://nova.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://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:36521 Tue 26 May 2020 10:11:49 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:44957 Tue 25 Oct 2022 12:35:30 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:51430 Tue 05 Sep 2023 17:47:25 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:34994 Thu 28 Oct 2021 13:04:29 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:30666 Thu 28 Oct 2021 13:04:12 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:54768 Mon 11 Mar 2024 15:08:11 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:51535 Fri 08 Sep 2023 12:31:27 AEST ]]>