https://nova.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:34998 Wed 02 Mar 2022 14:29:06 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:49445 Tue 16 May 2023 13:53:12 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:35330 Tue 16 Jul 2019 12:26:38 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:55863 Tue 02 Jul 2024 16:13:45 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:40012 Streptococcus pneumoniae, Haemophilus influenzae and Pseudomonas aeruginosa)to induce infection in both the respiratory and gastroin-testinal (GI) tracts. However, the importance and mechanism of HIF-1αin augmenting PAFR-dependent bacterial infections in COPD are poorly understood. Here, we review the evidence for the roles of local tissue hypoxia-induced inflammation, HIF-1α and PAFR in facilitating bacterial infections in COPD. Blocking PAFR may provide a novel antimicrobial approach to manage bacterial infections in COPD.]]> Fri 22 Jul 2022 13:06:35 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:40893 Streptococcus pneumoniae, non-typeable Haemophilus influenzae, Mycobacterium tuberculosis, Aspergillus fumigatus, etc., have the ability to elicit pro-oxidant pathways in the respiratory tract. Also, these pathogens are equipped with enzymatic and non-enzymatic mechanisms to neutralize host-associated oxidative molecules that facilitate the persistence of these pathogens in the lungs. We will discuss the CRD/pathogen-triggered oxidative stress in the lungs. We will also discuss the microbial mechanisms that may further increase oxidative stress in patients with CRDs that potentially results in the heightened inflammatory response in the lungs. Finally, we will discuss the current treatment strategies to limit the oxidative response-associated lung pathologies.]]> Fri 22 Jul 2022 10:38:45 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:38952 Haemophilus influenzae (NTHi), using immunofluorescence microscopy. In addition, expression of a known receptor of NTHi, platelet-activating factor receptor (PAFR), and two pro-inflammatory cytokines, interleukin 6 (IL-6) and interleukin-8 (IL-8), were determined using quantitative polymerase chain reaction. We observed a dose-dependent increase in NTHi adhesion to human bronchial epithelial cells following exposure to cow dung but not wood smoke extracts. Pre-treatment with PAFR antagonists, WEB-2086 and its analogue, C17, decreased adherence by NTHi to airway epithelial cells exposed to cow dung smoke. Both cow dung and wood smoke-induced expression of PAFR, as well as of IL-6 and IL-8, which was inhibited by WEB-2086 and C17. In conclusion, biomass smoke from combustion of cow dung and wood-induced expression of PAFR and airway inflammatory markers in human bronchial epithelial cells. Cow dung exposure, but not wood smoke exposure, mediated a measurable increase in NTHi adhesion to airway epithelial cells that was inhibited by PAFR antagonists. This work highlights the potential of PAFR as a therapeutic target for reducing the impact of hazardous biomass smoke exposure on respiratory health.]]> Fri 11 Mar 2022 14:48:35 AEDT ]]>