Format

Send to

Choose Destination
Am J Physiol Lung Cell Mol Physiol. 2019 Jul 1;317(1):L49-L56. doi: 10.1152/ajplung.00060.2019. Epub 2019 Apr 10.

Infants with evolving bronchopulmonary dysplasia demonstrate monocyte-specific expression of IL-1 in tracheal aspirates.

Author information

1
Division of Pulmonary and Sleep Medicine, Department of Pediatrics, University of Washington, Seattle, Washington.
2
Immunology Program, Benaroya Research Institute , Seattle, Washington.
3
Bioinformatics Program, Benaroya Research Institute , Seattle, Washington.
4
Center for Immunity and Immunotherapies, Seattle Children's Research Institute , Seattle, Washington.
5
Division of Neonatology, Department of Pediatrics, University of Washington , Seattle, Washington.

Abstract

Bronchopulmonary dysplasia (BPD) remains a devastating consequence of prematurity. Repeated inflammatory insults worsen lung injury, but there are no predictors for BPD-related respiratory outcomes or targeted therapies. We sought to understand inflammatory mechanisms in evolving BPD through molecular characterization of monocytes in tracheal aspirates from infants at risk for developing BPD. We performed flow cytometry targeting myeloid cell populations on prospectively collected tracheal aspirates from intubated patients born before 29 wk of gestation and <30 days old. We identified CD14+CD16+ (double-positive) and CD14+CD16- (single-positive) monocytes and characterized their gene expression profiles by RNA sequencing and quantitative PCR. We further analyzed differential gene expression between time points to evaluate changes in monocyte function over the first weeks of life. Expression of IL-1A, IL-1B, and IL-1 receptor antagonist mRNA was increased in monocytes collected at day of life (DOL) 7, DOL 14, and DOL 28 compared with those collected at DOL 3. This study suggests that early changes in monocyte-specific IL-1 cytokine pathways may be associated with evolving BPD.

KEYWORDS:

BPD; IL-1; RNASeq; monocyte

PMID:
30969811
DOI:
10.1152/ajplung.00060.2019

Supplemental Content

Full text links

Icon for Atypon
Loading ...
Support Center