https://nova.newcastle.edu.au/vital/access/ /manager/Index en-au 5 Obese asthmatics are characterized by altered adipose tissue macrophage activation https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:43499 Wed 21 Sep 2022 10:05:07 AEST ]]> Programming of the lung by early-life infection https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:15236 Wed 11 Apr 2018 17:06:49 AEST ]]> A pathogenic role for tumor necrosis factor-related apoptosis-inducing ligand in chronic obstructive pulmonary disease https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:21994 Thu 28 Oct 2021 12:36:38 AEDT ]]> Targeting PP2A and proteasome activity ameliorates features of allergic airway disease in mice 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 ]]> Mucosal production of uric acid by airway epithelial cells contributes to particulate matter-induced allergic sensitization https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:21993 Thu 14 Apr 2022 11:02:37 AEST ]]> Mucosal production of uric acid by airway epithelial cells contributes to particulate matter-induced allergic sensitization https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:29496 Thu 14 Apr 2022 10:58:05 AEST ]]> Tumor necrosis factor-related apoptosis-inducing ligand translates neonatal respiratory infection into chronic lung disease https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:14218 Sat 24 Mar 2018 08:24:47 AEDT ]]> Constitutive production of IL-13 promotes early-life Chlamydia respiratory infection and allergic airway disease https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:15982 -/- mice had reduced infection, inflammation, and mucus-secreting cell hyperplasia. Surprisingly, infection of wild-type (WT) mice did not increase IL-13 production but reduced IL-13Rα2 decoy receptor levels compared with sham-inoculated controls. Infection of WT but not Il13-/- mice induced persistent AHR. Infection and associated pathology were restored in infected Il13-/- mice by reconstitution with IL-13. Stat6-/- mice were also largely protected. Neutralization of IL-13 during infection prevented subsequent infection-induced severe AAD. Thus, early-life Chlamydia respiratory infection reduces IL-13Rα2 production, which may enhance the effects of constitutive IL-13 and promote more severe infection, persistent AHR, and AAD.]]> Sat 24 Mar 2018 08:23:40 AEDT ]]> Streptococcus pneumoniae infection suppresses allergic airways disease by inducing regulatory T-cells https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:13282 Sat 24 Mar 2018 08:15:15 AEDT ]]>