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Original Research: Bronchiectasis |

Is Alveolar Macrophage Phagocytic Dysfunction in Children With Protracted Bacterial Bronchitis a Forerunner to Bronchiectasis?

Sandra Hodge, PhD; John W. Upham, PhD; Susan Pizzutto, PhD; Helen L. Petsky, BN, PhD; Stephanie Yerkovich, MBiostats, PhD; Katherine J. Baines, PhD; Peter Gibson, MD; Jodie L. Simpson, PhD; Helen Buntain, PhD; Alice C.H. Chen, PhD; Greg Hodge, PhD; Anne B. Chang, PhD
Author and Funding Information

FUNDING/SUPPORT: This work was supported by the National Health and Medical Research Council (NHMRC), Australia (project grant 1042601); and the Channel 7 Children’s Research Foundation, Australia (grant 13688).

CORRESPONDENCE TO: Sandra Hodge, PhD, Chronic Inflammatory Lung Disease Research Laboratory, Lung Research Unit, Hanson Institute, Frome Rd, Adelaide, SA, Australia, 5001


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


Chest. 2016;149(2):508-515. doi:10.1016/j.chest.2015.10.066
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Background  Children with recurrent protracted bacterial bronchitis (PBB) and bronchiectasis share common features, and PBB is likely a forerunner to bronchiectasis. Both diseases are associated with neutrophilic inflammation and frequent isolation of potentially pathogenic microorganisms, including nontypeable Haemophilus influenzae (NTHi), from the lower airway. Defective alveolar macrophage phagocytosis of apoptotic bronchial epithelial cells (efferocytosis), as found in other chronic lung diseases, may also contribute to tissue damage and neutrophil persistence. Thus, in children with bronchiectasis or PBB and in control subjects, we quantified the phagocytosis of airway apoptotic cells and NTHi by alveolar macrophages and related the phagocytic capacity to clinical and airway inflammation.

Methods  Children with bronchiectasis (n = 55) or PBB (n = 13) and control subjects (n = 13) were recruited. Alveolar macrophage phagocytosis, efferocytosis, and expression of phagocytic scavenger receptors were assessed by flow cytometry. Bronchoalveolar lavage fluid interleukin (IL) 1β was measured by enzyme-linked immunosorbent assay.

Results  For children with PBB or bronchiectasis, macrophage phagocytic capacity was significantly lower than for control subjects (P = .003 and P < .001 for efferocytosis and P = .041 and P = .004 for phagocytosis of NTHi; PBB and bronchiectasis, respectively); median phagocytosis of NTHi for the groups was as follows: bronchiectasis, 13.7% (interquartile range [IQR], 11%-16%); PBB, 16% (IQR, 11%-16%); control subjects, 19.0% (IQR, 13%-21%); and median efferocytosis for the groups was as follows: bronchiectasis, 14.1% (IQR, 10%-16%); PBB, 16.2% (IQR, 14%-17%); control subjects, 18.1% (IQR, 16%-21%). Mannose receptor expression was significantly reduced in the bronchiectasis group (P = .019), and IL-1β increased in both bronchiectasis and PBB groups vs control subjects.

Conclusions  A reduced alveolar macrophage phagocytic host response to apoptotic cells or NTHi may contribute to neutrophilic inflammation and NTHi colonization in both PBB and bronchiectasis. Whether this mechanism also contributes to the progression of PBB to bronchiectasis remains unknown.

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