https://nova.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:52876 Wed 28 Feb 2024 11:01:07 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:55440 Thu 30 May 2024 15:41:44 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:51207 Thu 24 Aug 2023 15:00:51 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:43246 Thu 15 Sep 2022 10:17:31 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:46928 Thu 08 Dec 2022 12:25:53 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:36726 ɛ4/ɛ3> ɛ3/ɛ3> ɛ2/ɛ3> ɛ2/ɛ2). The greatest variation in lipids was related to the ɛ2 isoform, where various lysophosphatidylcholines and all phosphatidylethanolamine (PE) subclasses were elevated relative to ɛ3/ɛ3 and ɛ4 carriers. APOE ɛ4 carriers had reduced phosphatidylinositol relative to ɛ3/ɛ3 and ɛ2 carriers. Logistic regression revealed that ɛ2 carriers were at least 4 times higher odds of being in the highest tertile of PE lipid level relative to ɛ3/ɛ3. The elevation in PE and other phospholipids in ɛ2 carriers may indicate the protective effect of ɛ2 is linked to these phospholipids. Additionally, high baseline PE in cognitively normal participants predicted protection against cognitive decline six years later. Our data suggest substantial modulation of plasma lipids by APOE genotype and therefore indicates possible lipid targets and pathomechanisms involved in AD risk.]]> Thu 02 Jul 2020 09:10:42 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:27120 Sat 24 Mar 2018 07:41:34 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:32072 Mon 23 Sep 2019 10:24:40 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:37942 Acinetobacter baumannii. Our analyses reveal that AA and DHA incorporate into the A. baumannii bacterial membrane and impact bacterial fitness and membrane integrity, with DHA having a more pronounced effect. Through transcriptional profiling and mutant analyses, we show that the A. baumannii β-oxidation pathway plays a protective role against AA and DHA, by limiting their incorporation into the phospholipids of the bacterial membrane. Furthermore, our study identified a second bacterial membrane protection system mediated by the AdeIJK efflux system, which modulates the lipid content of the membrane via direct efflux of lipids other than AA and DHA, thereby providing a novel function for this major efflux system in A. baumannii This is the first study to examine the antimicrobial effects of host fatty acids on A. baumannii and highlights the potential of AA and DHA to protect against A. baumannii infections.Importance: A shift in the Western diet since the industrial revolution has resulted in a dramatic increase in the consumption of omega-6 fatty acids, with a concurrent decrease in the consumption of omega-3 fatty acids. This decrease in omega-3 fatty acid consumption has been associated with significant disease burden, including increased susceptibility to infectious diseases. Here we provide evidence that DHA, an omega-3 fatty acid, has superior antimicrobial effects upon the highly drug-resistant pathogen Acinetobacter baumannii, thereby providing insights into one of the potential health benefits of omega-3 fatty acids. The identification and characterization of two novel bacterial membrane protective mechanisms against host fatty acids provide important insights into A. baumannii adaptation during disease. Furthermore, we describe a novel role for the major multidrug efflux system AdeIJK in A. baumannii membrane maintenance and lipid transport. This core function, beyond drug efflux, increases the appeal of AdeIJK as a therapeutic target.]]> Mon 05 Jul 2021 16:17:04 AEST ]]>