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Paediatric lung disease
Original article
Carbon in airway macrophages from children with asthma
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  1. Rossa E Brugha1,
  2. Naseem Mushtaq1,
  3. Thomas Round1,
  4. Dev H Gadhvi1,
  5. Isobel Dundas1,
  6. Erol Gaillard2,
  7. Lee Koh1,
  8. Louise J Fleming3,
  9. Daniel J Lewis4,
  10. Marek Sanak5,
  11. Helen E Wood6,
  12. Benjamin Barratt6,
  13. Ian S Mudway6,
  14. Frank J Kelly6,
  15. Christopher J Griffiths1,
  16. Jonathan Grigg1
  1. 1Blizard Institute, Queen Mary, University of London, London, UK
  2. 2Department of Infection, Immunity and Inflammation, University Hospitals of Leicester, Leicester, UK
  3. 3Department of Respiratory Paediatrics, Imperial College, London, UK
  4. 4Department of Social and Environmental Health Research, London School of Hygiene and Tropical Medicine, London, UK
  5. 5Department of Medicine, Jagiellonian University Medical School, Krakow, Poland
  6. 6MRC-PHE Centre for Environment and Health, School of Biomedical Sciences, King's College London, UK
  1. Correspondence to Professor Jonathan Grigg, Centre for Paediatrics, Blizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary, University of London, 4 Newark Street, London E1 2AT, UK; j.grigg{at}qmul.ac.uk

Abstract

Background Airway macrophage (AM) phagocytosis is impaired in severe asthma. Prostaglandin (PG) E2 and D2 are increased in severe asthma and suppress AM phagocytic function in vitro. In this study, we sought evidence for PG-mediated impairment of phagocytosis of inhalable carbonaceous particulate matter (PM) by AM in children with severe asthma compared with mild asthmatics and healthy controls.

Methods AM were obtained from children with asthma and healthy controls using induced sputum. AM carbon area (μm2) was assessed by image analysis. In a subgroup of asthmatics, urinary PGE2 and PGD2 metabolites were measured by high-performance liquid chromatography, and PM exposure at the home address was modelled. Phagocytosis of PM by human monocyte-derived macrophages and rat AM was assessed in vitro by image analysis.

Results AM carbon was 51% lower in children with moderate-to-severe asthma (n=36) compared with mild asthmatics (n=12, p<0.01) and healthy controls (n=47, p<0.01). There was no association between modelled PM exposure and AM carbon in 33 asthmatics who had a urine sample, but there was an inverse association between AM carbon and urinary metabolites of PGE2 and D2 (n=33, rs=−0.40, p<0.05, and rs=−0.44, p<0.01). PGE2 10−6 M, but not PGD2 10−6 M, suppressed phagocytosis of PM10 by human macrophages in vitro (p<0.05 vs control). PGE2 10−6 M also suppressed phagocytosis of PM10 by rat AM in vitro (p<0.01 vs control).

Conclusions Phagocytosis of inhaled carbonaceous PM by AMs is impaired in severe asthma. PGE2 may contribute to impaired AM phagocytic function in severe asthma.

Keywords
  • Macrophage Biology

https://doi.org/10.1136/thoraxjnl-2013-204734

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