Interleukin-1 balance in the lungs of preterm infants who develop bronchopulmonary dysplasia.
BACKGROUND
The local pulmonary balance between the agonist and antagonist of interleukin-1 (IL-1) may influence the development of inflammatory disease and resultant structural damage in a variety of human diseases including adult respiratory distress syndrome and asthma.


OBJECTIVE
We tested the hypothesis that IL-1 cytokines are early markers for bronchopulmonary dysplasia (BPD), when measured in tracheal aspirates (TAs) obtained from premature infants being ventilated for respiratory distress syndrome during the first week of life.


METHODS
Serial TAs were collected on days 1, 3, 5 and 7 from 35 preterm infants (16 BPD, 19 non-BPD) in the absence of chorioamnionitis, and were assayed for IL-1 cytokines and leukocytes.


RESULTS
In spite of comparable maternal demographic and clinical characteristics, premature infants who developed BPD had higher levels of IL-1 receptor antagonist (Ra) in their airways on the first day of life. This antagonist IL-1Ra was an early and persistent marker for BPD during the first week of life. The agonist IL-1beta also increased significantly for BPD patients early, both compared to non-BPD patients, and also within the BPD group. While the early (day 1) IL-1 antagonist/agonist molar balance offered protection, by days 5 and 7, a threshold for IL-1Ra in the presence of increasing IL-1beta expression-favored pro-inflammation in the BPD group.


CONCLUSIONS
We conclude that a strong and early expression of airway antagonist (IL-1Ra) proves ultimately to be sub-optimal and non-protective due to the robust expression of airway agonist (IL-1beta) seen by day 5 in premature infants who develop BPD.
Kakkera
Deepika K
DK
Divisions of Neonatology, Departments of Pediatrics, State University of New York at Stony Brook, New York, NY, USA.
Siddiq
Mustafa M
MM
Parton
Lance A
LA
D001997:Bronchopulmonary Dysplasia / Q000378:metabolism*; D006801:Humans; D007231:Infant, Newborn; D007234:Infant, Premature; D053590:Interleukin 1 Receptor Antagonist Protein; D007375:Interleukin-1 / Q000032:analysis*; D008168:Lung / Q000737:chemistry*; D012121:Respiration, Artificial; D012127:Respiratory Distress Syndrome, Newborn / Q000378:metabolism / Q000628:therapy; D012795:Sialoglycoproteins / Q000032:analysis; D013396:Suction; D014132:Trachea
C507763:IL1RN protein, human; D053590:Interleukin 1 Receptor Antagonist Protein; D007375:Interleukin-1; D012795:Sialoglycoproteins