https://ogma.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 The complex interplay between endoplasmic reticulum stress and the NLRP3 inflammasome: a potential therapeutic target for inflammatory disorders https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:45088 Wed 26 Oct 2022 12:23:36 AEDT ]]> Elucidating novel disease mechanisms in severe asthma https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:30208 Wed 11 Apr 2018 11:33:34 AEST ]]> Interleukin-22 in urinary tract disease - new experimental directions https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:40146 Tue 05 Jul 2022 15:49:42 AEST ]]> Cord blood group 2 innate lymphoid cells are associated with lung function at 6 weeks of age https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:40658 Thu 28 Jul 2022 12:42:40 AEST ]]> Enhancing tristetraprolin activity reduces the severity of cigarette smoke-induced experimental chronic obstructive pulmonary disease https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:45028 Zfp36 gene is an anti‐inflammatory protein that induces mRNA decay, especially of transcripts encoding inflammatory cytokines, including those implicated in COPD. Methods: Here, we identify a novel protective role for TTP in CS‐induced experimental COPD using Zfp36aa/aa mice, a genetically modified mouse strain in which endogenous TTP cannot be phosphorylated, rendering it constitutively active as an mRNA‐destabilising factor. TTP wild‐type (Zfp36+/+) and Zfp36aa/aa active C57BL/6J mice were exposed to CS for four days or eight weeks, and the impact on acute inflammatory responses or chronic features of COPD, respectively, was assessed. Results: After four days of CS exposure, Zfp36aa/aa mice had reduced numbers of airway neutrophils and lymphocytes and mRNA expression levels of cytokines compared to wild‐type controls. After eight weeks, Zfp36aa/aa mice had reduced pulmonary inflammation, airway remodelling and emphysema‐like alveolar enlargement, and lung function was improved. We then used pharmacological treatments in vivo (protein phosphatase 2A activator, AAL(S), and the proteasome inhibitor, bortezomib) to promote the activation and stabilisation of TTP and show that hallmark features of CS‐induced experimental COPD were ameliorated. Conclusion: Collectively, our study provides the first evidence for the therapeutic potential of inducing TTP as a treatment for COPD.]]> Thu 27 Oct 2022 09:28:02 AEDT ]]> Unravelling the molecular basis for regulatory T-cell plasticity and loss of function in disease https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:37554 Thu 18 Feb 2021 09:43:20 AEDT ]]> Microbiome effects on immunity, health and disease in the lung https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:34690 Thu 03 Feb 2022 12:20:07 AEDT ]]> In vivo targeting of miR-223 in experimental eosinophilic oesophagitis https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:41570 Thu 02 May 2024 15:43:27 AEST ]]>