Transcriptional profiling of lung macrophages identifies a predictive signature for inflammatory lung disease in preterm infants View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2020-05-22

AUTHORS

Debashis Sahoo, Livia S. Zaramela, Gilberto E. Hernandez, Uyen Mai, Sahar Taheri, Dharanidhar Dang, Ashley N. Stouch, Rachel M. Medal, Alyssa M. McCoy, Judy L. Aschner, Timothy S. Blackwell, Karsten Zengler, Lawrence S. Prince

ABSTRACT

Lung macrophages mature after birth, placing newborn infants, particularly those born preterm, within a unique window of susceptibility to disease. We hypothesized that in preterm infants, lung macrophage immaturity contributes to the development of bronchopulmonary dysplasia (BPD), the most common serious complication of prematurity. By measuring changes in lung macrophage gene expression in preterm patients at risk of BPD, we show here that patients eventually developing BPD had higher inflammatory mediator expression even on the first day of life. Surprisingly, the ex vivo response to LPS was similar across all samples. Our analysis did however uncover macrophage signature genes whose expression increased in the first week of life specifically in patients resilient to disease. We propose that these changes describe the dynamics of human lung macrophage differentiation. Our study therefore provides new mechanistic insight into both neonatal lung disease and human developmental immunology. More... »

PAGES

259

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/s42003-020-0985-2

DOI

http://dx.doi.org/10.1038/s42003-020-0985-2

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1127792107

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/32444859


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27 schema:description Lung macrophages mature after birth, placing newborn infants, particularly those born preterm, within a unique window of susceptibility to disease. We hypothesized that in preterm infants, lung macrophage immaturity contributes to the development of bronchopulmonary dysplasia (BPD), the most common serious complication of prematurity. By measuring changes in lung macrophage gene expression in preterm patients at risk of BPD, we show here that patients eventually developing BPD had higher inflammatory mediator expression even on the first day of life. Surprisingly, the ex vivo response to LPS was similar across all samples. Our analysis did however uncover macrophage signature genes whose expression increased in the first week of life specifically in patients resilient to disease. We propose that these changes describe the dynamics of human lung macrophage differentiation. Our study therefore provides new mechanistic insight into both neonatal lung disease and human developmental immunology.
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34 analysis
35 birth
36 bronchopulmonary dysplasia
37 changes
38 common serious complication
39 complications
40 days
41 development
42 developmental immunology
43 differentiation
44 disease
45 dynamics
46 dysplasia
47 ex
48 expression
49 first day
50 first week
51 gene expression
52 genes
53 immaturity
54 immunology
55 infants
56 inflammatory lung diseases
57 inflammatory mediator expression
58 insights
59 life
60 lung disease
61 lung macrophages
62 macrophage differentiation
63 macrophage gene expression
64 macrophages
65 mechanistic insights
66 mediator expression
67 neonatal lung disease
68 new mechanistic insights
69 newborn infants
70 patients
71 predictive signature
72 prematurity
73 preterm
74 preterm infants
75 preterm patients
76 profiling
77 response
78 risk
79 risk of BPD
80 samples
81 serious complications
82 signature genes
83 signatures
84 study
85 susceptibility
86 transcriptional profiling
87 unique window
88 weeks
89 window
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