https://ogma.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:22168 -/-) BALB/c mice were intranasally sensitised and challenged with HDM prior to infection with RV1B. In some experiments, mice were administered recombinant IFN or adoptively transferred with plasmacytoid dendritic cells (pDC). Results: Allergic Tlr7^-/- mice displayed impaired IFN release upon RV1B infection, increased virus replication and exaggerated eosinophilic inflammation and airways hyper reactivity. Treatment with exogenous IFN or adoptive transfer of TLR7-competent pDCs blocked these exaggerated inflammatory responses and boosted IFNγ release in the absence of host TLR7 signalling. TLR7 expression in the lungs was suppressed by allergic inflammation and by interleukin (IL)-5-induced eosinophilia in the absence of allergy. Subjects with moderate-to-severe asthma and eosinophilic but not neutrophilic airways inflammation, despite inhaled steroids, showed reduced TLR7 and IFNλ2/3 expression in endobronchial biopsies. Furthermore, TLR7 expression inversely correlated with percentage of sputum eosinophils. Conclusions: This implicates IL-5-induced airways eosinophilia as a negative regulator of TLR7 expression and antiviral responses, which provides a molecular mechanism underpinning the effect of eosinophil-targeting treatments for the prevention of asthma exacerbations.]]> Wed 11 Apr 2018 15:36:21 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:14160 -/-), 4^-/- or 2/4^-/- BALB/c mice. Wt mice had moderate disease and infection. TLR2^-/- mice had more severe disease and more intense and prolonged infection compared to other groups. TLR4^-/- mice were asymptomatic. TLR2/4^-/- mice had severe early disease and persistent infection, which resolved thereafter consistent with the absence of symptoms in TLR4^-/- mice. Wt mice mounted robust innate and adaptive responses with an influx of natural killer (NK) cells, neutrophils, myeloid (mDCs) and plasmacytoid (pDCs) dendritic cells, and activated CD4⁺ and CD8⁺ T-cells into the lungs. Wt mice also had effective production of interferon (IFN)c in the lymph nodes and lung, and proliferation of lymph node T-cells. TLR2^-/- mice had more intense and persistent innate (particularly neutrophil) and adaptive cell responses and IL-17 expression in the lung, however IFNγ responses and T-cell proliferation were reduced. TLR2/4^-/- mice had reduced innate and adaptive responses. Most importantly, neutrophil phagocytosis was impaired in the absence of TLR2. Thus, TLR2 expression, particularly on neutrophils, is required for effective control of Chlamydia respiratory infection in early life. Loss of control of infection leads to enhanced but ineffective TLR4-mediated inflammatory responses that prolong disease symptoms. This indicates that TLR2 agonists may be beneficial in the treatment of early life Chlamydia infections and associated diseases.]]> Wed 11 Apr 2018 13:47:06 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:31941 Tue 10 Apr 2018 11:22:18 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:7560 Sat 24 Mar 2018 08:42:06 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:8036 Sat 24 Mar 2018 08:35:05 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:7272 Sat 24 Mar 2018 08:33:52 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:7255 Sat 24 Mar 2018 08:33:49 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:14649 Sat 24 Mar 2018 08:20:54 AEDT ]]> https://ogma.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://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:9915 Sat 24 Mar 2018 08:13:34 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:11486 Sat 24 Mar 2018 08:10:26 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:11164 Sat 24 Mar 2018 08:08:30 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:17510 Sat 24 Mar 2018 08:04:13 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:20102 Sat 24 Mar 2018 08:00:09 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:17737 Sat 24 Mar 2018 07:57:39 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:5132 Sat 24 Mar 2018 07:49:44 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:5135 Sat 24 Mar 2018 07:49:39 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:6617 Sat 24 Mar 2018 07:46:21 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:22279 Sat 24 Mar 2018 07:17:42 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:22164 Sat 24 Mar 2018 07:14:59 AEDT ]]>