https://nova.newcastle.edu.au/vital/access/ /manager/Index en-au 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:4425 Wed 11 Apr 2018 13:44:07 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:7255 Sat 24 Mar 2018 08:33:49 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:1061 Sat 24 Mar 2018 08:32:13 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:2202 Sat 24 Mar 2018 08:30:10 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:13276 + T cell cytokine production was abrogated. The adoptive transfer of TLR7-sufficient, but not TLR7-deficient pDC to TLR7 gene-deleted mice recapitulated the antiviral responses observed in wild-type mice and promoted virus clearance. In summary, TLR7-mediated signaling by pDC is required for appropriate innate responses to acute pneumovirus infection. It is conceivable that as-yet–unidentified defects in the TLR7 signaling pathway may be associated with elevated levels of RSV-associated morbidity and mortality among otherwise healthy human infants.]]> Sat 24 Mar 2018 08:15:16 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:17727 − ion conductance). Pharmacological analyses in vitro and in vivo determined that elevated Cl⁻ conductance is mediated by altered cystic fibrosis transmembrane conductance regulator expression and activity. Generation of iIL-13Tg/Il13rα1^−/−, iIL-13Tg/Il13rα2^−/−, and iIL-13Tg/Stat6^−/− mice revealed that IL-13-mediated dysregulation of epithelial architecture and Cl⁻ conductance is dependent on IL-13Rα1 and STAT-6. These observations demonstrate a central role for the IL-13/IL-13Rα1 pathway in the regulation of intestinal epithelial cell Cl⁻ secretion via up-regulation of cystic fibrosis transmembrane conductance regulator, suggesting an important role for this pathway in secretory diarrhea.]]> Sat 24 Mar 2018 07:57:45 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:22282 In vivo studies in mice with eotaxin and/or interleukin 5 (IL-5) deficiency showed that FI-RSV vaccination did not lead to enhanced pulmonary disease, where following challenge there were reduced pulmonary eosinophilia, inflammation, Th2-type cytokine responses, and altered chemokine (TARC and CCL17) responses. In contrast to wild-type mice, RSV was recovered at high titers from the lungs of eotaxin- and/or IL-5-deficient mice. Adoptive transfer of eosinophils to FI-RSV-immunized eotaxin- and IL-5-deficient (double-deficient) mice challenged with RSV was associated with potent viral clearance that was mediated at least partly through nitric oxide. These studies show that pulmonary eosinophilia has dual outcomes: one linked to RSV-induced airway inflammation and pulmonary pathology and one with innate features that contribute to a reduction in the viral load.]]> Sat 24 Mar 2018 07:17:42 AEDT ]]>