Is alveolar macrophage phagocytic dysfunction in children with protracted bacterial bronchitis a forerunner to bronchiectasis?

Hodge, Sandra, Upham, John W., Pizzutto, Susan, Petsky, Helen L., Yerkovich, Stephanie, Baines, Katherine J., Gibson, Peter, Simpson, Jodie L., Buntain, Helen, Chen, Alice C. H., Hodge, Greg and Chang, Anne B. (2016) Is alveolar macrophage phagocytic dysfunction in children with protracted bacterial bronchitis a forerunner to bronchiectasis?. Chest, 149 2: 508-515. doi:10.1016/j.chest.2015.10.066


Author Hodge, Sandra
Upham, John W.
Pizzutto, Susan
Petsky, Helen L.
Yerkovich, Stephanie
Baines, Katherine J.
Gibson, Peter
Simpson, Jodie L.
Buntain, Helen
Chen, Alice C. H.
Hodge, Greg
Chang, Anne B.
Title Is alveolar macrophage phagocytic dysfunction in children with protracted bacterial bronchitis a forerunner to bronchiectasis?
Journal name Chest   Check publisher's open access policy
ISSN 1931-3543
0012-3692
Publication date 2016-02-01
Year available 2016
Sub-type Article (original research)
DOI 10.1016/j.chest.2015.10.066
Open Access Status Not Open Access
Volume 149
Issue 2
Start page 508
End page 515
Total pages 8
Place of publication Glenview, IL, United States
Publisher American College of Chest Physicians
Collection year 2017
Language eng
Formatted abstract
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.
Keyword Bronchiectasis
Childhood lung disease
Inflammation
Macrophage
Phagocytosis
Protracted bacterial bronchitis
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
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