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Rhinovirus induction of fractalkine (CX3CL1) in airway and peripheral blood mononuclear cells in asthma.
PLoS One 2017; 12(8):e0183864Plos

Abstract

Rhinovirus infection is associated with the majority of asthma exacerbations. The role of fractalkine in anti-viral (type 1) and pathogenic (type 2) responses to rhinovirus infection in allergic asthma is unknown. To determine whether (1) fractalkine is produced in airway cells and in peripheral blood leucocytes, (2) rhinovirus infection increases production of fractalkine and (3) levels of fractalkine differ in asthmatic compared to non-asthmatic subjects. Fractalkine protein and mRNA levels were measured in bronchoalveolar lavage (BAL) cells and peripheral blood mononuclear cells (PBMCs) from non-asthmatic controls (n = 15) and mild allergic asthmatic (n = 15) subjects. Protein levels of fractalkine were also measured in macrophages polarised ex vivo to give M1 (type 1) and M2 (type 2) macrophages and in BAL fluid obtained from mild (n = 11) and moderate (n = 14) allergic asthmatic and non-asthmatic control (n = 10) subjects pre and post in vivo rhinovirus infection. BAL cells produced significantly greater levels of fractalkine than PBMCs. Rhinovirus infection increased production of fractalkine by BAL cells from non-asthmatic controls (P<0.01) and in M1-polarised macrophages (P<0.05), but not in BAL cells from mild asthmatics or in M2 polarised macrophages. Rhinovirus induced fractalkine in PBMCs from asthmatic (P<0.001) and healthy control subjects (P<0.05). Trends towards induction of fractalkine in moderate asthmatic subjects during in vivo rhinovirus infection failed to reach statistical significance. Fractalkine may be involved in both immunopathological and anti-viral immune responses to rhinovirus infection. Further investigation into how fractalkine is regulated across different cell types and into the effect of stimulation including rhinovirus infection is warranted to better understand the precise role of this unique dual adhesion factor and chemokine in immune cell recruitment.

Authors+Show Affiliations

Airway Disease Infection Section, National Heart & Lung Institute, Imperial College London, London, United Kingdom. MRC & Asthma UK Centre in Allergic Mechanisms of Asthma, London, United Kingdom. Randall Division of Cell and Molecular Biophysics, Kings College London, London, United Kingdom.Airway Disease Infection Section, National Heart & Lung Institute, Imperial College London, London, United Kingdom. MRC & Asthma UK Centre in Allergic Mechanisms of Asthma, London, United Kingdom. Imperial College Healthcare NHS Trust, London, United Kingdom.NRC institute of Immunology FMBA, Moscow, Russian Federation. Mechnikov Research Institute for Vaccines and Sera, Moscow, Russian Federation.Respiratory Infection Section, National Heart and Lung Institute, Imperial College London, London, United Kingdom.NRC institute of Immunology FMBA, Moscow, Russian Federation.Airway Disease Infection Section, National Heart & Lung Institute, Imperial College London, London, United Kingdom. MRC & Asthma UK Centre in Allergic Mechanisms of Asthma, London, United Kingdom. Imperial College Healthcare NHS Trust, London, United Kingdom.Airway Disease Infection Section, National Heart & Lung Institute, Imperial College London, London, United Kingdom. MRC & Asthma UK Centre in Allergic Mechanisms of Asthma, London, United Kingdom.Airway Disease Infection Section, National Heart & Lung Institute, Imperial College London, London, United Kingdom. MRC & Asthma UK Centre in Allergic Mechanisms of Asthma, London, United Kingdom. Imperial College Healthcare NHS Trust, London, United Kingdom.Airway Disease Infection Section, National Heart & Lung Institute, Imperial College London, London, United Kingdom. MRC & Asthma UK Centre in Allergic Mechanisms of Asthma, London, United Kingdom. Imperial College Healthcare NHS Trust, London, United Kingdom. Respiratory Infection Section, National Heart and Lung Institute, Imperial College London, London, United Kingdom.Imperial College Healthcare NHS Trust, London, United Kingdom.Imperial College Healthcare NHS Trust, London, United Kingdom.Airway Disease Infection Section, National Heart & Lung Institute, Imperial College London, London, United Kingdom. MRC & Asthma UK Centre in Allergic Mechanisms of Asthma, London, United Kingdom.Airway Disease Infection Section, National Heart & Lung Institute, Imperial College London, London, United Kingdom. MRC & Asthma UK Centre in Allergic Mechanisms of Asthma, London, United Kingdom. Imperial College Healthcare NHS Trust, London, United Kingdom.Airway Disease Infection Section, National Heart & Lung Institute, Imperial College London, London, United Kingdom. MRC & Asthma UK Centre in Allergic Mechanisms of Asthma, London, United Kingdom. Imperial College Healthcare NHS Trust, London, United Kingdom.Airway Disease Infection Section, National Heart & Lung Institute, Imperial College London, London, United Kingdom. MRC & Asthma UK Centre in Allergic Mechanisms of Asthma, London, United Kingdom. Imperial College Healthcare NHS Trust, London, United Kingdom.Airway Disease Infection Section, National Heart & Lung Institute, Imperial College London, London, United Kingdom. MRC & Asthma UK Centre in Allergic Mechanisms of Asthma, London, United Kingdom.Airway Disease Infection Section, National Heart & Lung Institute, Imperial College London, London, United Kingdom. MRC & Asthma UK Centre in Allergic Mechanisms of Asthma, London, United Kingdom. Imperial College Healthcare NHS Trust, London, United Kingdom.Airway Disease Infection Section, National Heart & Lung Institute, Imperial College London, London, United Kingdom. MRC & Asthma UK Centre in Allergic Mechanisms of Asthma, London, United Kingdom. Imperial College Healthcare NHS Trust, London, United Kingdom.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

28859129

Citation

Upton, Nadine, et al. "Rhinovirus Induction of Fractalkine (CX3CL1) in Airway and Peripheral Blood Mononuclear Cells in Asthma." PloS One, vol. 12, no. 8, 2017, pp. e0183864.
Upton N, Jackson DJ, Nikonova AA, et al. Rhinovirus induction of fractalkine (CX3CL1) in airway and peripheral blood mononuclear cells in asthma. PLoS ONE. 2017;12(8):e0183864.
Upton, N., Jackson, D. J., Nikonova, A. A., Hingley-Wilson, S., Khaitov, M., Del Rosario, A., ... Sykes, A. (2017). Rhinovirus induction of fractalkine (CX3CL1) in airway and peripheral blood mononuclear cells in asthma. PloS One, 12(8), pp. e0183864. doi:10.1371/journal.pone.0183864.
Upton N, et al. Rhinovirus Induction of Fractalkine (CX3CL1) in Airway and Peripheral Blood Mononuclear Cells in Asthma. PLoS ONE. 2017;12(8):e0183864. PubMed PMID: 28859129.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Rhinovirus induction of fractalkine (CX3CL1) in airway and peripheral blood mononuclear cells in asthma. AU - Upton,Nadine, AU - Jackson,David J, AU - Nikonova,Alexandra A, AU - Hingley-Wilson,Suzie, AU - Khaitov,Musa, AU - Del Rosario,Ajerico, AU - Traub,Stephanie, AU - Trujillo-Torralbo,Maria-Belen, AU - Habibi,Max, AU - Elkin,Sarah L, AU - Kon,Onn M, AU - Edwards,Michael R, AU - Mallia,Patrick, AU - Footitt,Joseph, AU - Macintyre,Jonathan, AU - Stanciu,Luminita A, AU - Johnston,Sebastian L, AU - Sykes,Annemarie, Y1 - 2017/08/31/ PY - 2016/11/14/received PY - 2017/08/12/accepted PY - 2017/9/1/entrez PY - 2017/9/1/pubmed PY - 2017/10/17/medline SP - e0183864 EP - e0183864 JF - PloS one JO - PLoS ONE VL - 12 IS - 8 N2 - Rhinovirus infection is associated with the majority of asthma exacerbations. The role of fractalkine in anti-viral (type 1) and pathogenic (type 2) responses to rhinovirus infection in allergic asthma is unknown. To determine whether (1) fractalkine is produced in airway cells and in peripheral blood leucocytes, (2) rhinovirus infection increases production of fractalkine and (3) levels of fractalkine differ in asthmatic compared to non-asthmatic subjects. Fractalkine protein and mRNA levels were measured in bronchoalveolar lavage (BAL) cells and peripheral blood mononuclear cells (PBMCs) from non-asthmatic controls (n = 15) and mild allergic asthmatic (n = 15) subjects. Protein levels of fractalkine were also measured in macrophages polarised ex vivo to give M1 (type 1) and M2 (type 2) macrophages and in BAL fluid obtained from mild (n = 11) and moderate (n = 14) allergic asthmatic and non-asthmatic control (n = 10) subjects pre and post in vivo rhinovirus infection. BAL cells produced significantly greater levels of fractalkine than PBMCs. Rhinovirus infection increased production of fractalkine by BAL cells from non-asthmatic controls (P<0.01) and in M1-polarised macrophages (P<0.05), but not in BAL cells from mild asthmatics or in M2 polarised macrophages. Rhinovirus induced fractalkine in PBMCs from asthmatic (P<0.001) and healthy control subjects (P<0.05). Trends towards induction of fractalkine in moderate asthmatic subjects during in vivo rhinovirus infection failed to reach statistical significance. Fractalkine may be involved in both immunopathological and anti-viral immune responses to rhinovirus infection. Further investigation into how fractalkine is regulated across different cell types and into the effect of stimulation including rhinovirus infection is warranted to better understand the precise role of this unique dual adhesion factor and chemokine in immune cell recruitment. SN - 1932-6203 UR - https://www.unboundmedicine.com/medline/citation/28859129/Rhinovirus_induction_of_fractalkine__CX3CL1__in_airway_and_peripheral_blood_mononuclear_cells_in_asthma_ L2 - http://dx.plos.org/10.1371/journal.pone.0183864 DB - PRIME DP - Unbound Medicine ER -