https://ogma.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 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:16824 Wed 11 Apr 2018 09:44:48 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:15980 Sat 24 Mar 2018 08:23:40 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:15983 50% of asthma-related healthcare costs. New investigations into the pathogenesis of glucocorticoid resistance in severe asthma indicate that pulmonary macrophages may play central roles in promoting airway inflammation, particularly in asthma that is resistant to steroid therapy. Importantly, factors that are linked to the activation of pulmonary macrophages may contribute to glucocorticoid resistance and severe asthma. Here, we review recent advances in understanding the roles of pulmonary macrophages in the mechanisms of glucocorticoid resistance and the pathogenesis of severe asthma. We discuss the role of macrophage phenotype, infection, IFN-γ, LPS, associated signaling pathways, TNF-α, MIF, and other macrophage-associated factors. Understanding the pathogenesis of steroid-resistant severe asthma will contribute to the identification of optimal therapeutic strategies for the effective management of the disease.]]> Sat 24 Mar 2018 08:23:36 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:18254 Sat 24 Mar 2018 08:04:34 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:25080 Fri 01 Apr 2022 09:27:01 AEDT ]]>