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Lung-Resident Pericytes Acquire Increased Migratory Capacity in a House Dust Mite-Driven Model of Asthma
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A5798 - Lung-Resident Pericytes Acquire Increased Migratory Capacity in a House Dust Mite-Driven Model of Asthma
Author Block: J. Johnson1, J. E. Rowley2; 1School of Life and Health Sciences, Aston University, Birmingham, United Kingdom, 2National Heart and Lung Institute, Imperial College London, London, United Kingdom.
RATIONALE: Asthma is characterized by structural changes such as airway smooth muscle (ASM) thickening and fibrosis. Our previous studies have shown that, in the murine house dust mite (HDM) model of allergic airway disease, pericytes detach from the airway microvasculature and contribute to airway remodeling by transforming into myofibroblasts; however, the mechanisms driving pericyte migration from the microvasculature to areas of inflammation and fibrosis are not fully understood. Pericytes are vascular mural cells that maintain vascular homeostasis but are also considered to be tissue-resident mesenchymal stem cells (MSC). AIM: To assess the migratory capacity of lung pericytes in a mouse model chronic of airway inflammation. Furthermore, to establish changes in the expression of cell surface markers associated with migration in pericytes in the healthy and inflamed lung. HYPOTHESIS: Under conditions of chronic allergic inflammation, lung pericytes will express chemokine receptors at higher levels and display enhanced migratory capacity.
METHODS: Flow cytometric analysis was performed on pericytes (CD45/CD31/Ter119-, CD146hi, PDGFRβ+) isolated from the murine lung. Purified pericytes were then subjected to in vitro migration assays. Lung sections from healthy and HDM-exposed mice were also assessed for chemokine receptor expression.
RESULTS: Flow cytometry revealed that pericytes increase their expression of the chemokine receptor CXCR4, and increased CXCR4 expression was also observed on pericytes that had accumulated in the airway wall of mice exposed to HDM. Furthermore, pericytes obtained from the lungs of HDM-exposed mice displayed enhanced migratory capacity to a range of mediators in Transwell assays compared to pericytes from the lungs of healthy mice.
CONCLUSIONS: Pulmonary pericytes are local resident MSC that demonstrate enhanced migratory capacity in the context of chronic allergic inflammation driven by HDM exposure. CXCR4+ pericytes contribute to airway remodeling in response to chronic aeroallergen exposure.
Author Block: J. Johnson1, J. E. Rowley2; 1School of Life and Health Sciences, Aston University, Birmingham, United Kingdom, 2National Heart and Lung Institute, Imperial College London, London, United Kingdom.
RATIONALE: Asthma is characterized by structural changes such as airway smooth muscle (ASM) thickening and fibrosis. Our previous studies have shown that, in the murine house dust mite (HDM) model of allergic airway disease, pericytes detach from the airway microvasculature and contribute to airway remodeling by transforming into myofibroblasts; however, the mechanisms driving pericyte migration from the microvasculature to areas of inflammation and fibrosis are not fully understood. Pericytes are vascular mural cells that maintain vascular homeostasis but are also considered to be tissue-resident mesenchymal stem cells (MSC). AIM: To assess the migratory capacity of lung pericytes in a mouse model chronic of airway inflammation. Furthermore, to establish changes in the expression of cell surface markers associated with migration in pericytes in the healthy and inflamed lung. HYPOTHESIS: Under conditions of chronic allergic inflammation, lung pericytes will express chemokine receptors at higher levels and display enhanced migratory capacity.
METHODS: Flow cytometric analysis was performed on pericytes (CD45/CD31/Ter119-, CD146hi, PDGFRβ+) isolated from the murine lung. Purified pericytes were then subjected to in vitro migration assays. Lung sections from healthy and HDM-exposed mice were also assessed for chemokine receptor expression.
RESULTS: Flow cytometry revealed that pericytes increase their expression of the chemokine receptor CXCR4, and increased CXCR4 expression was also observed on pericytes that had accumulated in the airway wall of mice exposed to HDM. Furthermore, pericytes obtained from the lungs of HDM-exposed mice displayed enhanced migratory capacity to a range of mediators in Transwell assays compared to pericytes from the lungs of healthy mice.
CONCLUSIONS: Pulmonary pericytes are local resident MSC that demonstrate enhanced migratory capacity in the context of chronic allergic inflammation driven by HDM exposure. CXCR4+ pericytes contribute to airway remodeling in response to chronic aeroallergen exposure.
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