https://nova.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:31237 Wed 09 Feb 2022 15:56:28 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:51803 Tue 19 Sep 2023 15:01:59 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:28587 Tue 08 Jan 2019 15:13:51 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:21994 Thu 28 Oct 2021 12:36:38 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:48625 p = .04). Infant acute-care presentations (45 versus 13%, p = .02) and oral corticosteroid use (26 versus 4%, p = .03) due to “asthma/wheezing” were higher in the maternal group with 25(OH)D < 75 nmol/L, versus ≥75 nmol/L. Conclusions: Most pregnant women with asthma had low vitamin D status, which persisted across gestation. Low maternal vitamin D status was associated with greater risk of adverse respiratory outcomes in their infants, a group at high risk of developing childhood asthma.]]> Thu 23 Mar 2023 18:39:19 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:14218 Sat 24 Mar 2018 08:24:47 AEDT ]]> 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 ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:19723 Sat 24 Mar 2018 07:53:42 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:21359 Sat 24 Mar 2018 07:51:24 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:48275 Mon 13 Mar 2023 19:05:36 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:24090 Aspergillus fumigatus allergen mouse model of EoE. Because IL-33 induction was transient in this model and chronicity of IL-33 expression has been demonstrated in humans, naive mice were treated with recombinant IL-33 for 1 wk and esophageal pathology was evaluated. IL-33 application produced changes consistent with phenotypically early EoE, including transmural eosinophilia, mucosal hyperproliferation, and upregulation of eosinophilic genes and chemokines. Th2 cytokines, including IL-13, along with innate lymphoid cell group 2, Th1/17, and M2 macrophage marker genes, were increased after IL-33 application. IL-33-induced eosinophilia was ablated in IL-13 null mice. In addition, IL-33 induced a profound inhibition of the regulatory T cell gene signature. We conclude that IL-33 gene expression is associated with pediatric EoE development and that application of recombinant protein in mice phenocopies the early clinical phase of the human disease in an IL-13-dependent manner. IL-33 inhibition of esophageal regulatory T cell function may induce loss of antigenic tolerance, thereby providing a mechanistic rationale for EoE development.]]> Fri 03 Dec 2021 10:32:37 AEDT ]]>