https://nova.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:51026 Wed 28 Feb 2024 16:13:12 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:53765 Wed 28 Feb 2024 15:59:45 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:50532 Wed 28 Feb 2024 15:56:07 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:45438 Wed 20 Mar 2024 15:45:49 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:53717 Wed 10 Jan 2024 11:16:55 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:34994 Thu 28 Oct 2021 13:04:29 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:39670 Thu 28 Jul 2022 08:10:20 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:50895 Thu 10 Aug 2023 10:29:50 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:32991 In utero exposure to particulate matter (PM) from a range of sources is associated with adverse post-natal health; however, the effect of maternal exposure to community-sampled PM on early post-natal lung and immune development is poorly understood. Objectives: Using a mouse model, we aimed to determine whether in utero exposure to PM alters early post-natal lung function and immune cell populations. We used PM collected from ceiling voids in suburban houses as a proxy for community PM exposure. Methods: Pregnant C57BL/6 mice were intranasally exposed to ceiling derived PM, or saline alone, at gestational day (E) 13.5, 15.5, and 17.5. When mice were two weeks old, we assessed lung function by the forced oscillation technique, and enumerated T and B cell populations in the spleen and thymus by flow cytometry. Results: Maternal exposure to PM impaired somatic growth of male offspring resulting in reduced lung volume and deficits in lung function. There was no effect on thymic T cell populations in dams and their male offspring but PM decreased the CD4 +CD25 + T cell population in the female offspring. In contrast, maternal exposure to PM increased splenic CD3 +CD4 + and CD3 +CD8 + T cells in dams, and there was some evidence to suggest inhibition of splenic T cell maturation in male but not female offspring. Conclusions: Our findings suggested that maternal exposure to ceiling void PM has the capacity to impair early somatic growth and alter early life immune development in a sex specific manner.]]> Thu 03 Feb 2022 12:19:29 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:26099 TM Western assays. Transepithelial permeability assays were performed to assess effects on barrier functionality. RT2 Profiler focused qPCR arrays and pathway analysis evaluating associations between human TJ and antiviral response were performed to identify potential interactions and pathways between genes of interests. Results: HRV-1B infection affected viability that was both time and TCID⁵⁰ dependent. Significant increases in apoptosis and viral replication post-infection correlated with viral titer. Viral infection significantly decreased claudin-1 protein expression at the lower TCID⁵⁰, while a significant decrease in all three TJ protein expressions occurred at higher TCID⁵⁰. Decrease in protein expression was concomitant with significant increases in epithelial permeability of fluorescein isothiocynate labeled-dextran 4 and 20 kDa. Analysis of focused qPCR arrays demonstrated a significant decrease in ZO-1 gene expression. Furthermore, network analysis between human TJ and antiviral response genes revealed possible interactions and regulation of TJ genes via interleukin (IL)-15 in response to HRV-1B infection. Conclusion: HRV-1B infection directly alters human airway epithelial TJ expression leading to increased epithelial permeability potentially via an antiviral response of IL-15.]]> Sat 24 Mar 2018 07:39:52 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:29058 Sat 24 Mar 2018 07:37:18 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:53947 Mon 22 Jan 2024 16:56:55 AEDT ]]> 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 ]]>