https://nova.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:48714 Wed 29 Mar 2023 17:10:48 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:38039 Wed 28 Jul 2021 09:42:45 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:53093 Wed 28 Feb 2024 16:21:51 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:51134 Wed 28 Feb 2024 16:20:04 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:50124 Wed 28 Feb 2024 16:17:49 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:50653 Wed 28 Feb 2024 15:55:38 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:51924 Wed 28 Feb 2024 09:57:50 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:47500 Wed 24 Jan 2024 14:49:50 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:43527 Wed 21 Sep 2022 11:32:49 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:49965 Wed 21 Jun 2023 11:57:33 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:36481 Wed 20 May 2020 16:22:43 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:36606 Wed 17 Nov 2021 16:31:32 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:39137 Wed 13 Mar 2024 13:58:54 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:17148 Wed 11 Apr 2018 17:15:05 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:16713 Wed 11 Apr 2018 17:02:19 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:31124 Wed 11 Apr 2018 16:45:05 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:23281 Wed 11 Apr 2018 16:20:11 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:21083 Wed 11 Apr 2018 14:39:15 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:25152 Wed 11 Apr 2018 13:49:07 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:26497 Wed 11 Apr 2018 12:26:15 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:27102 Wed 11 Apr 2018 11:30:17 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:14773 Wed 11 Apr 2018 11:04:31 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:13988 Wed 11 Apr 2018 10:50:22 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:27878 Wed 11 Apr 2018 10:26:27 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:23627 Wed 11 Apr 2018 10:17:52 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:36433 + neutrophils as median fluorescence intensity (MFI). Results: Neutrophil surface expression of CD62L was significantly reduced in COPD (median (IQR) MFI: 1156 (904, 1365)) compared with asthma (1865 (1157, 2408)) and healthy controls (2079 (1054, 2960)); p=0.028. COPD neutrophils also demonstrated a significant reduction in CD62L expression with and without fMLF stimulation. Asthma participants had a significantly increased proportion and number of CD62L^bright/CD16^dim neutrophils (median: 5.4% and 0.14 x 10⁹/L, respectively), in comparison with healthy (3.54% and 0.12 x 10⁹/L, respectively); p<0.017. Conclusion: Reduced CD62L expression suggests blood neutrophils have undergone priming in COPD but not in asthma, which may be the result of systemic inflammation. The increased shedding of CD62L receptor by COPD blood neutrophils suggests a high sensitivity for activation]]> Wed 10 Nov 2021 15:05:07 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:31235 HI monocytes/macrophages and neutrophils. Body weight and clinical scores were recorded throughout the experiment. Results: We demonstrate that KB treatment attenuated cigarette smoke-induced lung inflammation as shown by reductions in levels of BAL IFNγ, CXCL9, CXCL10, CCL5, IL-6, G-CSF, and IL-17. KB additionally attenuated the quantity of BAL lymphocytes and macrophages. In parallel to the attenuation of lung inflammation, KB induced a systemic immune activation with increases in Ly6C^HI monocytes/macrophages and neutrophils. Conclusions: This is the first demonstration that subcutaneous administration of a microbial-based immunotherapy can attenuate cigarette smoke-induced lung inflammation, and modulate BAL lymphocyte and macrophage levels, while inducing a systemic immune activation and mobilization. These data provide a foundation for future studies exploring how KB may be used to either reverse or prevent progression of established emphysema and small airways disease associated with chronic cigarette smoke exposure. The data suggest the intriguing possibility that KB, which stimulates rather than suppresses systemic immune responses, might be a novel means by which the course of COPD pathogenesis may be altered.]]> Wed 10 Nov 2021 15:05:01 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:41455 Wed 10 Aug 2022 12:11:24 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:29974 2) COPD patients received a 12 week weight reduction programme involving meal replacements, dietary counselling by a dietitian and resistance exercise training prescribed and supervised by a physiotherapist. Patients were reviewed face to face by the dietitian and physiotherapist every 2 weeks for counselling. Results: Twenty-eight participants completed the intervention. Mean (standard deviation) body mass index was 36.3 kg/m2 (4.6) at baseline and reduced by 2.4 kg/m2 ((1.1) P < 0.0001) after the intervention. Importantly, skeletal muscle mass was maintained. Clinical outcomes improved with weight loss including exercise capacity, health status, dyspnea, strength and functional outcomes. There was also a significant reduction in the body mass index, obstruction, dyspnea and exercise score (BODE). Systemic inflammation measured by C-reactive protein however did not change. Conclusion: In obese COPD patients, dietary energy restriction coupled with resistance exercise training results in clinically significant improvements in body mass index, exercise tolerance and health status, whilst preserving skeletal muscle mass. This novel study provides a framework for development of guidelines for the management of obese COPD patients and in guiding future research.]]> Wed 09 Mar 2022 15:59:32 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:50285 Wed 06 Mar 2024 14:18:15 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:34285 Wed 06 Apr 2022 13:57:14 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:30933 Wed 04 Sep 2019 09:54:22 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:33179 1 < 80% predicted to those with an FEV₁ > 80% predicted after bronchodilator use. In the population with an FEV₁< 80%, analysis was further stratified based on smoking history. Results: Omalizumab treatment markedly improved asthma control and health-related quality of life in all populations assessed based on the Asthma Control Questionnaire and Asthma Quality of Life Questionnaire scores. Omalizumab treatment did not improve lung function (FEV₁, FVC, or FEV₁/FVC ratio) in populations that were enriched for asthma-COPD overlap (diagnosis of COPD or FEV₁ < 80%/ever smokers). Conclusions: Our study suggests that omalizumab improves asthma control and health-related quality of life in individuals with severe allergic asthma and overlapping COPD. These findings provide real-world efficacy data for this patient population and suggest that omalizumab is useful in the management of severe asthma with COPD overlap.]]> Wed 04 Sep 2019 09:48:23 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:19319 55 years) with obstructive airway disease and healthy controls (N=56) underwent inhaler technique assessment, skin allergy testing, venepuncture, fractional exhaled nitric oxide (FENO) and gas diffusion measurement, exercise testing, sputum induction, and questionnaire assessment. They then completed an assessment burden questionnaire across five domains: difficulty, discomfort, pain, symptoms and test duration. Results: Test perception was generally favourable. Induced sputum had the greatest test burden perceived as being more difficult (mean 0.83, P=0.001), associated with more discomfort (mean 1.3, P<0.001), more painful (0.46, P=0.019), longer test duration (0.84, P<0.001) and worsening symptoms (0.55, P=0.001) than the questionnaires. FENO had a more favourable assessment but was assessed to be difficult to perform. Inhaler technique received the most favourable assessment. Conclusions: Older adults hold favourable perceptions to a range of tests that they might encounter in the course of their care for airway disease. The newer tests of sputum induction and FENO have some observed difficulties, in particular sputum induction. The results of this study can inform current practice by including details of the test and its associated adverse effects when conducting the test, as well as providing clear explanations of the utility of tests and how the results might aid in patient care.]]> Tue 26 Jun 2018 11:28:14 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:42445 1% predicted) and consumption of fried fish (OR -0.12, 95% CI -0.22, -0.01, P = 0.026) but not fish prepared by other cooking methods or estimated intakes of PUFA. There was no association between fish or PUFA intakes and COPD risk. Compared to age and sex matched controls, cases had poorer lung function and a higher rate of smoking prevalence but did not differ in their intakes of fish or PUFA or their PUFA levels in plasma phospholipids. In this sub-population, we found a marginally significant association between COPD risk and total long chain n-3PUFA levels in plasma phospholipids (OR 1.22 95% CI 1.00-1.49, P = 0.046). Given the relatively small number of cases in this analysis, this finding should be interpreted with caution, especially given the lack of association with other markers of n-3PUFA intake or status. Taken together, our data suggest that n-3PUFA intake and status are not determinants of improved lung function in this regional Australian population.]]> Tue 23 Aug 2022 10:54:28 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:53295 Tue 21 Nov 2023 11:54:41 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:54312 Tue 20 Feb 2024 14:27:17 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:51001 Tue 15 Aug 2023 12:06:35 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:50999 Tue 15 Aug 2023 11:52:40 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:13502 Tue 11 Dec 2018 15:40:19 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:36564 Tue 09 Jun 2020 13:09:47 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:31397 IL1R1, IL1R2, and IL1RN), and signaling molecules (IRAK2, IRAK3, and PELI1), were measured in sputum using real-time quantitative polymerase chain reaction. Mediators were compared between the frequent (≥2 exacerbations in the 12 months) and infrequent exacerbators, and the predictive relationships investigated using receiver operating characteristic curves and area under the curve (AUC) values. Results: Of the 95 participants, 89 completed the exacerbation follow-up, where 30 participants (n=22 COPD, n=8 asthma) had two or more exacerbations. At the baseline visit, expressions of IRAK2, IRAK3, PELI1, and IL1R1 were elevated in participants with frequent exacerbations of both asthma and COPD combined and separately. In the combined population, sputum gene expression of IRAK3 (AUC=75.4%; P<0.001) was the best predictor of future frequent exacerbations, followed by IL1R1 (AUC=72.8%; P<0.001), PELI1 (AUC=71.2%; P<0.001), and IRAK2 (AUC=68.6; P=0.004). High IL-1 pathway gene expression was associated with frequent prior year exacerbations and correlated with the number and severity of exacerbations. Conclusion: The upregulation of IL-1 pathway mediators is associated with frequent exacerbations of obstructive airway disease. Further studies should investigate these mediators as both potential diagnostic biomarkers predicting at-risk patients and novel treatment targets]]> Thu 28 Oct 2021 13:03:38 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:45138 Thu 27 Oct 2022 14:07:39 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:45323 Thu 27 Oct 2022 08:02:08 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:37731 Thu 27 Jan 2022 15:57:18 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:29098 Thu 26 Jul 2018 13:16:42 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:38305 Thu 26 Aug 2021 11:11:37 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:41709 Thu 25 Aug 2022 10:06:29 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:30509 18 years) with obesity (body mass index; BMI = 30 kg/m²) and COPD, using a low-calorie diet coupled with a partial meal replacement plan and resistance exercise training, which resulted in a 6.4% reduction in weight while maintaining skeletal muscle mass and improving health status. This sub-study aims to evaluate the intervention by (a) examining changes in dietary intake and nutritional biomarkers and (b) examining predictors of weight loss. Dietary intake was evaluated using four-day food diaries, and analysis of plasma fatty acids and plasma carotenoids as biomarkers of dietary fat intake and fruit and vegetable intake, respectively. Twenty-eight obese COPD subjects (n = 17 males, n = 11 females) with a mean (standard deviation; SD) age of 67.6 (6.3) years completed the 12-week weight loss intervention. Pre-intervention, mean (SD) BMI was 36.3 (4.6) kg/m². Micronutrient intake improved from pre- to post-intervention, with the percentage of subjects meeting the Nutrient Reference Values increased for all micronutrients. Post-intervention, significant decreases in total (p = 0.009) and saturated fat intake (p = 0.037), and corresponding decreases in total (p = 0.007) and saturated plasma fatty acids (p = 0.003) were observed. There was a trend towards higher total carotenoids post-intervention (p = 0.078). Older age (p = 0.025), higher pre-intervention uncontrolled eating (p < 0.001) and plasma carotenoids (p = 0.009) predicted weight loss. This demonstrates the efficacy of a weight loss intervention in improving diet quality of obese COPD adults.]]> Thu 24 Mar 2022 11:34:09 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:34512 Thu 17 Mar 2022 14:40:35 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:35998 Thu 17 Mar 2022 14:39:42 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:34955 Thu 17 Feb 2022 09:32:05 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:39902 Thu 14 Jul 2022 12:11:05 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:39904 Thu 14 Jul 2022 11:58:51 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:35868 Thu 14 Apr 2022 11:01:33 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:49876 3 mg/L), and depression. In both trials, TT treatment led to a large, significant improvement in HRQOL compared with usual care (Cohen's d = 1.19; P < .001). Receiving a statin for systemic inflammation and oral corticosteroid for eosinophilic airway inflammation was associated with the largest HRQOL improvements. Treatments for exercise intolerance, anxiety, and obesity were associated with smaller improvements in HRQOL. Conclusions: This study contributes to identifying clinically impactful TTs by showing that TTs across pulmonary, extrapulmonary, and behavioral domains were associated with HRQOL impairment and treatment response.]]> Thu 08 Jun 2023 15:21:50 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:46931 Thu 08 Dec 2022 11:32:09 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:52258 Thu 05 Oct 2023 14:13:27 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:36808 Thu 04 Nov 2021 10:39:56 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:36651 Haemophilus influenzae (NTHi) preparation was demonstrated in the mid-1980s. Subsequently, studies aiming to validate clinical efficacy of this oral treatment were complicated by a number of factors, including the modification of clinical definitions, the implications of which were not recognized at that time. The objective of this review is to integrate our pre-clinical and clinical research in this field conducted over the past 30 years to demonstrate the evolution of the idea of communication between mucosal surfaces through the common mucosal immune system and the development of an effective oral NTHi immunotherapy. Our earliest studies recruited subjects with chronic sputum production and high levels of culture-positive sputum for Gram-negative bacteria but by 2000, the clinical diagnostic focus had switched from "chronic bronchitis" to "chronic obstructive pulmonary disease" (COPD), which was functionally defined using spirometry. This change led to variable clinical trial results, confirming the importance of chronic sputum production and culture-positive sputum. Additional conditioning factors such as patient age and gender were influential in study populations with low culture-positive sputum production. Through this period, studies in human and in rodent models provided new insights into airway protection mechanisms and the pathogenesis of airway inflammation. Key findings were the importance of a dysbiosis within the airway microbiome, and the critical role of an interdependence between the bronchus and the gut, with a Peyer's patch-dependent extra-bronchus "loop" controlling the composition of the bronchus microbiome. Within this context, intercurrent virus infections initiate a microbiome-dependant hypersensitivity reaction involving Peyer's patch-derived Th17 cells. We conclude that whole-cell killed NTHi immunotherapy has consistent and significant benefits when examined in the context of changing clinical disease definitions, age and gender, and has the potential to change the natural history of chronic airway disease.]]> Thu 04 Nov 2021 10:39:51 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:30756 Thu 03 Feb 2022 12:22:32 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:29068 Thu 03 Feb 2022 12:20:12 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:29773 Haemophilus influenzae (NTHi) vaccine in chronic obstructive pulmonary disease (COPD): severe COPD, moderate-severe exacerbations as end-point and a threshold prevalence of NTHi in the study population. More data are needed to confirm parameters that influence clinical outcomes. Aims: The primary aim was to determine the efficacy of an oral NTHi vaccine (HI-164OV) in reducing the rate of exacerbations requiring systemic corticosteroids or hospitalisation in COPD. Secondary aims included effect on the proportion of patients experiencing such exacerbations, severity of infections and quality of life (St George Respiratory Questionnaire for COPD patients (SGRQ-C)). Methods: This multi-centre, double-blind, placebo-controlled study was conducted at 21 Australian sites for 9 months in 2011. Results: Three-hundred and twenty subjects with COPD, FEV₁ <60% predicted and ≥1 moderate-severe exacerbations in the previous 12 months were recruited. The primary and secondary end-points for the intention-to-treat population aged 40-88 years were not achieved, and only 5% of subjects had an H. influenzae-positive sputum sample. Subsequent exploratory analysis of patients <65years (91 subjects) indicated protection with respect to the primary and most of the secondary end-points, with SGRQ-C symptom scores lower at 3 and 6 months. Conclusion: Patients aged 40-88 years with moderate to severe COPD and low rates of H. influenzae-positive sputum were not protected against exacerbations by HI-1640V. Further studies are needed to confirm protection in subjects aged <65years. Older age and low colonisation rates appear to affect adversely response to this vaccine.]]> Thu 03 Feb 2022 12:18:55 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:46840 Thu 01 Dec 2022 15:50:25 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:46830 Thu 01 Dec 2022 11:45:24 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:35358 Thu 01 Aug 2019 15:34:56 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:14580 Sat 24 Mar 2018 08:22:41 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:14652 Sat 24 Mar 2018 08:19:13 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:18875 Sat 24 Mar 2018 08:03:15 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:19120 Sat 24 Mar 2018 07:55:57 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:28283 Sat 24 Mar 2018 07:41:21 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:26603 Sat 24 Mar 2018 07:33:57 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:28982 Sat 24 Mar 2018 07:29:26 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:26966 Sat 24 Mar 2018 07:26:59 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:21998 Sat 24 Mar 2018 07:14:33 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:22110 Sat 24 Mar 2018 07:13:17 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:39031 1 as have pericytes² and endothelial-mesenchymal transition.^3,4 However, the most studied mechanism is epithelial-mesenchymal transition (EMT), in which epithelial cells lose epithelial characteristics and become more mesenchymal, gaining mobility and enhanced ability to secrete ECM. This highly dynamic process has been subcategorized according to the three main functions it is associated with: embryonic development (type I), wound healing and tissue repair (type II), and cancer (type III). In this translational review, the mechanisms, roles, and impact of EMT (particularly type II) in chronic lung diseases are discussed. We also evaluate whether current medications influence EMT and how we may affect this process in the future.]]> Mon 29 Jan 2024 17:51:32 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:36167 Mon 26 Oct 2020 11:55:19 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:35633 Mon 23 Sep 2019 16:38:58 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:53927 Mon 22 Jan 2024 16:48:54 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:22044 Chlamydia, Haemophilus influenzae and Streptococcus pneumoniae in early life may promote permanent deleterious changes in immunity, lung structure, and function that predispose to, or increase the severity of chronic respiratory diseases in later life. For example, these infections increase immune responses, which drive subsequent asthma pathogenesis. Targeting the pathways involved with specific inhibitors or agonists may prevent these consequences of early-life infection. Vaccination and immunomodulatory therapies that control the infections and their sequelae may also be efficacious.]]> Mon 01 Feb 2016 13:04:15 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:41270 Mon 01 Aug 2022 09:49:29 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:37427 Fri 31 Mar 2023 15:03:59 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:48632 Fri 24 Mar 2023 10:57:01 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:38008 Fri 23 Jul 2021 15:13:02 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:48458 Fri 17 Mar 2023 12:07:53 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:47212 Fri 16 Dec 2022 10:09:29 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:51749 Fri 15 Sep 2023 18:21:52 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:35612 Fri 13 Sep 2019 16:49:42 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:41804 Fri 12 Aug 2022 12:31:50 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:46061 in vitro in human airway epithelial cell cultures and in vivo in mouse models of ICS administration. Mice deficient in the type I IFN-α/β receptor (Ifnar1^-/-) and administration of exogenous IFN-β were used to study the functional role of type-I interferon signaling in ACE2 expression. We compared sputum ACE2 expression in patients with COPD stratified according to use or nonuse of ICS. Results: ICS administration attenuated ACE2 expression in mice, an effect that was reversed by exogenous IFN-β administration, and Ifnar1^-/- mice had reduced ACE2 expression, indicating that type I interferon contributes mechanistically to this effect. ICS administration attenuated expression of ACE2 in airway epithelial cell cultures from patients with COPD and in mice with elastase-induced COPD-like changes. Compared with ICS nonusers, patients with COPD who were taking ICSs also had reduced sputum expression of ACE2. Conclusion: ICS therapies in COPD reduce expression of the SARS-CoV-2 entry receptor ACE2. This effect may thus contribute to altered susceptibility to COVID-19 in patients with COPD.]]> Fri 11 Nov 2022 14:22:05 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:30102 Fri 11 Jun 2021 13:30:23 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:38377 Fri 10 Sep 2021 12:38:35 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:28184 Fri 10 Mar 2023 17:09:31 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:14805 Fri 02 Nov 2018 14:20:43 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:33085 -/-) and TLR4-deficient (Tlr4^-/-) mice. CS-induced airway fibrosis, characterized by increased collagen deposition around small airways, was not altered in Tlr2^-/- mice but was attenuated in Tlr4^-/- mice compared with CS-exposed WT controls. However, Tlr2^-/- mice had increased CS-induced emphysema-like alveolar enlargement, apoptosis, and impaired lung function, while these features were reduced in Tlr4^-/- mice compared with CS-exposed WT controls. Taken together, these data highlight the complex roles of TLRs in the pathogenesis of COPD and suggest that activation of TLR2 and/or inhibition of TLR4 may be novel therapeutic strategies for the treatment of COPD.]]> Fri 01 Apr 2022 09:24:33 AEDT ]]>