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Original Research: Asthma |

Airway Surfactant Protein D Deficiency in Adults With Severe Asthma

Rose-Marie A. Mackay, PhD; Christopher L. Grainge, MD, PhD; Laurie C. Lau, PhD; Clair Barber, BSc; Howard W. Clark, MD, DPhil; Peter H. Howarth, MD, DM
Author and Funding Information

FUNDING/SUPPORT: This work was funded by the following grants: Wessex Severe Asthma Cohort Medical Research Council grant [code G0800649] and A Life Course Approach to Investigating Asthma Pathogenesis and Progression Medical Research Council grant [code G0900453].

CORRESPONDENCE TO: Rose-Marie A. Mackay, PhD, University of Southampton, Faculty of Medicine, Department of Child Health, Southampton General Hospital, Tremona Rd, Southampton SO16 7YD, UK


Copyright 2016, American College of Chest Physicians. All Rights Reserved.


Chest. 2016;149(5):1165-1172. doi:10.1016/j.chest.2015.11.012
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Background  Surfactant protein D (SP-D) is an essential component of the innate immune defense against pathogens within the airways. SP-D also regulates allergic inflammation and promotes the removal of apoptotic cells. SP-D dysregulation is evident in several pulmonary diseases. Our aim was to investigate whether airway and serum levels of SP-D are altered in treatment-resistant severe asthma.

Methods  SP-D concentrations were measured in matched serum and BAL samples collected from 10 healthy control subjects (HC) and 50 patients with asthma (22 with mild asthma [MA] and 28 with severe asthma [SA]). These samples were also evaluated by using Western blot analysis to investigate variations in SP-D size.

Results  SP-D levels in BAL samples were significantly lower in SA compared with HC and MA (P < .001) and inversely correlated with BAL eosinophil cationic protein concentrations in SA (P < .01). Serum SP-D was significantly increased in SA compared with HC and MA (P < .001), and BAL/serum ratios were significantly lower in SA compared with HC and MA (P < .001). Reduced SP-D levels in BAL samples, with concomitant increases in serum in SA, were associated with degraded fragments of SP-D in the serum and increased BAL neutrophil counts and lipopolysaccharide levels.

Conclusions  These findings suggest defective innate immunity within the airways in SA, as reflected by low BAL SP-D concentrations and altered bacterial presence with airway neutrophilia. Furthermore, BAL SP-D leakage into the serum in patients with SA may provide a peripheral blood biomarker, reflecting increased epithelial damage and/or epithelial permeability within the peripheral airways.

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