Carbon in airway macrophages from children with asthma
654 - 659
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Background: Airway macrophage (AM) phagocytosis is impaired in severe asthma. Prostaglandin (PG) E 2 and D 2 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 (μm 2 ) was assessed by image analysis. In a subgroup of asthmatics, urinary PGE 2 and PGD 2 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 PGE 2 and D 2 (n=33, rs=-0.40, p < 0.05, and rs=-0.44, p < 0.01). PGE 2 10 -6 M, but not PGD 2 10 -6 M, suppressed phagocytosis of PM 10 by human macrophages in vitro (p < 0.05 vs control). PGE 2 10 -6 M also suppressed phagocytosis of PM 10 by rat AM in vitro (p < 0.01 vs control). Conclusions: Phagocytosis of inhaled carbonaceous PM by AMs is impaired in severe asthma. PGE 2 may contribute to impaired AM phagocytic function in severe asthma.