Abdullah A Tarique1, Peter D Sly2, Diana G Cardenas1, Lin Luo3, Jennifer L Stow3, Scott C Bell4, Claire E Wainwright5, Emmanuelle Fantino1. 1. Child Health Research Centre (CHRC), The University of Queensland, Australia. 2. Child Health Research Centre (CHRC), The University of Queensland, Australia; Department of Respiratory and Sleep Medicine, Children's Health Queensland, Brisbane, Australia. Electronic address: p.sly@uq.edu.au. 3. Institute for Molecular Bioscience (IMB) and IMB Centre for Inflammation and Disease Research, The University of Queensland, Australia. 4. QIMR Berghofer Medical Research Institute, Brisbane, Australia; Department of Thoracic Medicine, The Prince Charles Hospital, Brisbane, Australia. 5. Child Health Research Centre (CHRC), The University of Queensland, Australia; Department of Respiratory and Sleep Medicine, Children's Health Queensland, Brisbane, Australia.
Abstract
INTRODUCTION: We previously reported defective alternative polarization (M2) of macrophages and early expression of classically polarized (M1) macrophage markers in unpolarized monocyte-derived macrophages (MDMs) in patients with cystic fibrosis (CF). The present study assessed whether the mechanism(s) underlying defective macrophage polarization resided in circulating monocytes. METHODS: Monocyte subsets (classical, intermediate and non-classical), markers for monocyte activation (CD163) and recruitment (CD195), receptors/genes associated with macrophage differentiation and polarization were analyzed in CF and compared with healthy individuals. RESULTS: No differences were observed in the monocyte subsets or in the expression of CD163 or CD195. Expression of the M-CSF receptor, TLR4, γC, IL-4Rα, IL-13Rα1, TIMP-1 and Cox-2 were higher in CF monocytes, albeit at low levels, whereas, LRP1, MMP9, MMP28 were downregulated compared to mooncytes from healthy individuals. CONCLUSIONS: Our data suggest that differences in CF monocytes may contribute to the reported CFTR-dependent defect in macrophage differentiation, polarization and function. Crown
INTRODUCTION: We previously reported defective alternative polarization (M2) of macrophages and early expression of classically polarized (M1) macrophage markers in unpolarized monocyte-derived macrophages (MDMs) in patients with cystic fibrosis (CF). The present study assessed whether the mechanism(s) underlying defective macrophage polarization resided in circulating monocytes. METHODS: Monocyte subsets (classical, intermediate and non-classical), markers for monocyte activation (CD163) and recruitment (CD195), receptors/genes associated with macrophage differentiation and polarization were analyzed in CF and compared with healthy individuals. RESULTS: No differences were observed in the monocyte subsets or in the expression of CD163 or CD195. Expression of the M-CSF receptor, TLR4, γC, IL-4Rα, IL-13Rα1, TIMP-1 and Cox-2 were higher in CF monocytes, albeit at low levels, whereas, LRP1, MMP9, MMP28 were downregulated compared to mooncytes from healthy individuals. CONCLUSIONS: Our data suggest that differences in CF monocytes may contribute to the reported CFTR-dependent defect in macrophage differentiation, polarization and function. Crown
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