https://nova.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:14499 Wed 11 Apr 2018 10:21:55 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:46022 300 inflammatory genes were similarly regulated in the uterine endometrium by mating independently of paternal diet, and 13 were dysregulated by HFD-fed compared with CD-fed males. Seminal vesicle fluid factors reduced in HFD-fed males, including TGF-β1, IL-10, and TNF, were among the predicted upstream regulators of differentially regulated genes. Additionally, the T-cell response induced by mating with CD-fed males was blunted after mating with HFD-fed males, with 27% fewer CD4⁺ T cells, 26% fewer FOXP3⁺CD4⁺ regulatory T cells (Treg) cells, and 19% fewer CTLA4⁺ Treg cells, particularly within the NRP1⁺ thymic Treg cell population. These findings demonstrate that an obesogenic HFD alters the composition of seminal vesicle fluid and impairs seminal plasma capacity to elicit a favorable pro-tolerogenic immune response in females at conception.]]> Wed 09 Nov 2022 11:05:03 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:49105 Tue 14 Nov 2023 14:40:06 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:27734 Thu 28 Oct 2021 13:04:05 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:48411 Thu 16 Mar 2023 14:04:16 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:30164 Thu 04 Nov 2021 10:38:29 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:33752 Thu 03 Feb 2022 12:18:24 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:1493 Sat 24 Mar 2018 08:28:05 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:12415 + lymphocytes (Th2 cells) and their cytokines predominate in mild to moderate allergic asthma, whereas severe steroid-resistant asthma has more of a mixed Th2/Th1 phenotype with a Th17 component. Other immune cells, particularly neutrophils, macrophages and dendritic cells, as well structural cells such as epithelial and airway smooth muscle cells also produce disease-associated cytokines in asthma. Increased levels of these immune cells and cytokines have been identified in clinical samples and their potential role in disease demonstrated in studies using mouse models of asthma. Clinical trials with inhibitors of cytokines such as interleukin (IL)-4, -5 and tumour necrosis factor-α have had success in some studies but not others. This may reflect the design of the clinical trials, including treatments regimes and the patient population included in these studies. IL-13, -9 and granulocyte-macrophage colony-stimulating factor are currently being evaluated in clinical trials or preclinically and the outcome of these studies is eagerly awaited. Roles for IL-25, -33, thymic stromal lymphopoietin, interferon-γ, IL-17 and -27 in the regulation of asthma are just emerging, identifying new ways to treat inflammation. Careful interpretation of results from mouse studies will inform the development and application of therapeutic approaches for asthma. The most effective approaches may be combination therapies that suppress multiple cytokines and a range of redundant and disconnected pathways that separately contribute to asthma pathogenesis. Astute application of these approaches may eventually lead to the development of effective asthma therapeutics. Here we review the current state of knowledge in the field.]]> Sat 24 Mar 2018 08:14:54 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:11118 Sat 24 Mar 2018 08:07:48 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:20104 Sat 24 Mar 2018 08:00:08 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:16896 Sat 24 Mar 2018 07:58:48 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:21530 Sat 24 Mar 2018 07:50:26 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:5597 Sat 24 Mar 2018 07:49:21 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:132 Sat 24 Mar 2018 07:43:12 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:28359 in vivo in the absence of allergen. Post hoc analysis of gene array data demonstrated significant upregulation of TRAIL and MID1 in a cohort of children with EoE compared with that seen in controls. Conclusion TRAIL regulates MID1 and TSLP, inflammation, fibrosis, smooth muscle hypertrophy, and expression of inflammatory effector chemokines and cytokines in experimental EoE.]]> Sat 24 Mar 2018 07:25:13 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:22161 Sat 24 Mar 2018 07:14:59 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:32284 Mon 23 Sep 2019 10:58:58 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:34081 Fri 27 Sep 2019 10:22:06 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:33088 H2 cells), their associated cytokines, and eosinophils in the regulation of hallmark features of allergic asthma. Notably, we consider the complexity of type-2 responses and studies that have explored integrated signaling among classical T_H2 cytokines (IL-4, IL-5, and IL-13), which together with CCL11 (eotaxin-1) regulate critical aspects of eosinophil recruitment, allergic inflammation, and airway hyper-responsiveness (AHR). Among our most important findings, we have provided evidence that the initiation of T_H2 responses is regulated by airway epithelial cell-derived factors, including TRAIL and MID1, which promote T_H2 cell development via STAT6-dependent pathways. Further, we highlight studies demonstrating that microRNAs are key regulators of allergic inflammation and potential targets for anti-inflammatory therapy. On the background of T_H2 inflammation, we have demonstrated that innate immune cells (notably, airway macrophages) play essential roles in the generation of steroid-resistant inflammation and AHR secondary to allergen- and pathogen-induced exacerbations. Our work clearly indicates that understanding the diversity and spatiotemporal role of the inflammatory response and its interactions with resident airway cells is critical to advancing knowledge on asthma pathogenesis and the development of new therapeutic approaches.]]> Fri 24 Aug 2018 16:27:29 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:37674 Fri 12 Mar 2021 10:01:58 AEDT ]]>