https://nova.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:51883 Wed 28 Feb 2024 15:48:29 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:51822 Wed 28 Feb 2024 09:21:14 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:24717 50 years old; n = 45). Thirteen (36.1%) reproductive-aged females were using the OCP. Participants had induced sputum cell counts measured and blood analysed for sex hormones and inflammatory markers. Results: Obese reproductive-aged females had higher sputum %neutrophils than nonobese reproductive-aged females (45.4 ± 24.3% vs 27.5 ± 17.5%, P = 0.016); however, there was no difference in sputum neutrophils in obese compared with nonobese males (P = 0.620) or older females (P = 0.087). Multiple linear regression analysis found testosterone and OCP use to be negative predictors of sputum %neutrophils, while C-reactive protein and IL-6 were positive predictors of sputum %neutrophils. BMI and age were not significant predictors in the multivariate model. Reproductive-aged females using the OCP had significantly lower sputum %neutrophils than those not using the OCP (23.2 ± 12.6% vs 42.1 ± 23.8%, P = 0.015). Conclusions: This study suggests that sex hormones and systemic inflammation may be mediating the obese-asthma phenotype. The observation that OCP use was associated with lower sputum %neutrophils in reproductive-aged females warrants further investigation.]]> Wed 09 Mar 2022 16:03:50 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:34729 Wed 09 Mar 2022 15:59:45 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:49859 Wed 07 Jun 2023 10:25:30 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:44806 Wed 01 May 2024 12:05:04 AEST ]]> 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:40080 Tue 05 Jul 2022 08:35:39 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:54560 Thu 29 Feb 2024 10:27:50 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:33082 (S)), or inhibiting proteasome activity with bortezomib (BORT), could suppress experimental AAD. Methods: Acute AAD was induced in C57BL/6 mice by intraperitoneal sensitization with ovalbumin (OVA) in combination with intranasal (i.n) exposure to OVA. Chronic AAD was induced in mice with prolonged i.n exposure to crude house dust mite (HDM) extract. Mice were treated with vehicle, FTY720, AAL_(S), BORT or AAL_(S)+- BORT and hallmark features of AAD assessed. Results: AAL_(S) reduced the severity of acute AAD by suppressing tissue eosinophils and inflammation, mucus-secreting cell (MSC) numbers, type 2-associated cytokines (interleukin (IL)-33, thymic stromal lymphopoietin, IL-5 and IL-13), serum immunoglobulin (Ig)E and airway hyper-responsiveness (AHR). FTY720 only suppressed tissue inflammation and IgE. BORT reduced bronchoalveolar lavage fluid (BALF) and tissue eosinophils and inflammation, IL-5, IL-13 and AHR. Combined treatment with AAL_(S)+BORT had complementary effects and suppressed BALF and tissue eosinophils and inflammation, MSC numbers, reduced the production of type 2 cytokines and AHR. AAL (S) , BORT and AAL (S) +BORT also reduced airway remodelling in chronic AAD. Conclusion: These findings highlight the potential of combination therapies that enhance PP2A and inhibit proteasome activity as novel therapeutic strategies for asthma.]]> Thu 17 Mar 2022 14:36:39 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:49306 Thu 11 May 2023 14:32:33 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:38659 Mon 29 Jan 2024 17:49:38 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:40140 Mon 25 Jul 2022 09:00:17 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:46346 via NF-κB, eicosanoid biosynthesis via the lipoxygenase pathway and IL-2 biosynthesis (all P<.01). Sputum macrophage number and the ES for most macrophage signatures were higher in the TAC3 group compared to TAC1 and TAC2 asthmatics. However, a high enrichment was found in TAC1 for 3 modules showing inflammatory pathways linked to Toll-like and TNF receptor activation and arachidonic acid metabolism (P<.001) and in TAC2 for the inflammasome and interferon signalling pathways (P<.001). Data were validated in the ADEPT cohort. Module analysis provides additional information compared to conventional M1 and M2 classification. TR-Mφ were enriched in TAC3 and associated with mitochondrial function. Conclusions: Macrophage activation is attenuated in severe granulocytic asthma highlighting defective innate immunity except for specific subsets characterized by distinct inflammatory pathways.]]> Fri 18 Nov 2022 10:08:37 AEDT ]]>