https://ogma.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:23760 4 (LXA,sub>4) can also interact with ALX/FPR2 receptors and lead to allosteric inhibition of SAA-initiated epithelial responses (pA₂ 13 nM). During acute exacerbation, peripheral blood SAA levels increased dramatically and were disproportionately increased relative to LXA₄. Human lung macrophages (CD68⁺) colocalized with SAA and GCs markedly increased SAA in vitro (THP-1, pEC₅₀ 43 nM). To determine its direct actions, SAA was administered into murine lung, leading to induction of CXC chemokine ligand 1/2 and a neutrophilic response that was inhibited by 15-epi-LXA₄ but not dexamethasone. Taken together, these findings identify SAA as a therapeutic target for inhibition and implicate SAA as a mediator of GC-resistant lung inflammation that can overwhelm organ protective signaling by lipoxins at ALX/FPR2 receptors.]]> Sat 24 Mar 2018 07:11:08 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:49505 Fri 19 May 2023 14:07:55 AEST ]]>