Abstract
BackgroundThe etiology of persistent lung inflammation in preterm infants with chronic lung disease of prematurity (CLD) is poorly characterized, hampering efforts to stratify prognosis and treatment. Airway macrophages are important innate immune cells with roles in both the induction and resolution of tissue inflammation.ObjectivesTo investigate airway innate immune cellular phenotypes in preterm infants with respiratory distress syndrome (RDS) or CLD.MethodsBronchoalveolar lavage (BAL) fluid was obtained from term and preterm infants requiring mechanical ventilation. BAL cells were phenotyped by flow cytometry.ResultsPreterm birth was associated with an increase in the proportion of non-classical CD14+/CD16+ monocytes on the day of delivery (58.9±5.8% of total mononuclear cells in preterm vs 33.0±6.1% in term infants, p = 0.02). Infants with RDS were born with significantly more CD36+ macrophages compared with the CLD group (70.3±5.3% in RDS vs 37.6±8.9% in control, p = 0.02). At day 3, infants born at a low gestational age are more likely to have greater numbers of CD14+ mononuclear phagocytes in the airway (p = 0.03), but fewer of these cells are functionally polarized as assessed by HLA-DR (p = 0.05) or CD36 (p = 0.05) positivity, suggesting increased recruitment of monocytes or a failure to mature these cells in the lung.ConclusionsThese findings suggest that macrophage polarization may be affected by gestational maturity, that more immature macrophage phenotypes may be associated with the progression of RDS to CLD and that phenotyping mononuclear cells in BAL could predict disease outcome.
Highlights
Chronic lung disease (CLD) of prematurity, often called bronchopulmonary dysplasia (BPD), is a significant complication of preterm birth, leading to increased respiratory symptoms, repeated hospital admissions and abnormal long term lung physiology resulting in great economic cost and markedly increased parental burden
These findings suggest that macrophage polarization may be affected by gestational maturity, that more immature macrophage phenotypes may be associated with the progression of respiratory distress syndrome (RDS) to chronic lung disease of prematurity (CLD) and that phenotyping mononuclear cells in Bronchoalveolar lavage (BAL) could predict disease outcome
Since CD14 is downregulated as macrophages mature [3], macrophage numbers were assessed both by CD14 and HLA-DR or CD36 coexpression and as HLA-DR/CD36 single stained events, the latter to account for CD14 low macrophages
Summary
Chronic lung disease (CLD) of prematurity, often called bronchopulmonary dysplasia (BPD), is a significant complication of preterm birth, leading to increased respiratory symptoms, repeated hospital admissions and abnormal long term lung physiology resulting in great economic cost and markedly increased parental burden. The pathogenesis of CLD is linked to a number of clinical factors, including prematurity, mechanical ventilation, oxygen therapy and post- and ante-natal infection all of which help to initiate or sustain an inflammatory process in the preterm lung. Persistent airway neutrophilia and elevated levels of neutrophil chemoattractants, including CXCL8, in bronchoalveolar lavage (BAL) fluid, are associated with the development of CLD in preterm infants [1]. Macrophages play important roles in inducing and resolving neutrophilic inflammation but their role in CLD is not well defined, in view of the difficulty in acquiring samples from significantly preterm infants. Unresolved questions are how the preterm infant lung orchestrates this inflammatory response and the role of macrophage populations in this process. The etiology of persistent lung inflammation in preterm infants with chronic lung disease of prematurity (CLD) is poorly characterized, hampering efforts to stratify prognosis and treatment. Airway macrophages are important innate immune cells with roles in both the induction and resolution of tissue inflammation
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