https://nova.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:45003 n = 19), including 7 with NEA and healthy controls (n = 10) underwent a clinical assessment, venepuncture and sputum induction. MDMs were co-cultured with apoptotic granulocytes isolated from healthy donors with or without exogenous recombinant galectin-3 (50 μg/mL) and efferocytosis was assessed by flow cytometry. Galectin-3 expression and localisation in MDMs was visualised by immunofluorescence staining and fluorescence microscopy. Galectin-3, interleukin (IL)-6 and CXCL8 secretion were measured in cell culture supernatants by ELISA and cytometric bead array. Results: Baseline efferocytosis (mean (±standard deviation)) was lower in participants with asthma (33.2 (±17.7)%) compared with healthy controls (45.3 (±15.9)%; p = 0.081). Efferocytosis did not differ between the participants with eosinophilic asthma (EA) (31.4 (±19.2)%) and NEA (28.7 (±21.5)%; p = 0.748). Addition of galectin-3 significantly improved efferocytosis in asthma, particularly in NEA (37.8 (±18.1)%) compared with baseline (30.4 (±19.7)%; p = 0.012). Efferocytosis was not associated with any of the clinical outcomes but was negatively correlated with sputum macrophage numbers (Spearman r = − 0.671; p = 0.017). Galectin-3 was diffusely distributed in most MDMs but formed punctate structures in 5% of MDMs. MDM galectin-3 secretion was lower in asthma (9.99 (2.67, 15.48) ng/mL) compared with the healthy controls (20.72 (11.28, 27.89) ng/mL; p = 0.044) while IL-6 and CXCL8 levels were similar. Conclusions: Galectin-3 modulates macrophage function in asthma, indicating a potential role for galectin-3 to reverse impaired efferocytosis in NEA.]]> Wed 26 Oct 2022 09:42:24 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:13589 Wed 11 Apr 2018 16:34:21 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:17053 Wed 11 Apr 2018 15:00:47 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: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:45364 Thu 27 Oct 2022 15:35:45 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:45097 Thu 27 Oct 2022 13:58:29 AEDT ]]> 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:29462 IRAKM, PCDH1, ORMDL3/GSDMB, IL-33, CDHR3 and CST1 in airway epithelial cells. Recent studies on epigenetic regulatory factors have further provided novel insights to the field, particularly their effect on regulation of some of the asthma susceptibility genes (e.g. methylation of ADAM33). Among the epigenetic regulatory mechanisms, microRNA networks have been shown to regulate a major portion of post-transcriptional gene regulation. Particularly, miR-19a may have some therapeutic potential.]]> Thu 24 Mar 2022 11:32:30 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:55056 Fri 05 Apr 2024 14:28:53 AEDT ]]>