Format

Send to

Choose Destination
See comment in PubMed Commons below
Pediatr Pulmonol. 2013 Jan;48(1):8-13. doi: 10.1002/ppul.22540. Epub 2012 Mar 19.

IFN-γ and IP-10 in tracheal aspirates from premature infants: relationship with bronchopulmonary dysplasia.

Author information

1
Department of Pediatrics, Cooper University Hospital, Camden, New Jersey, USA.

Abstract

BACKGROUND:

Interferon-gamma (IFN-γ) and interferon-inducible protein of 10 kDa (IP-10) are potent inflammatory mediators and contribute to acute lung injury in adults. Recently, a potential role for IFN-γ and IP-10 in the pathogenesis of bronchopulmonary dysplasia (BPD) has been reported in animal models.

OBJECTIVE:

To study the association between IFN-γ and IP-10 in tracheal aspirate (TA) and the development of BPD in premature infants.

DESIGN/METHODS:

TA samples collected within 48 hr after birth from 79 mechanically ventilated premature neonates [gestational age (GA) <30 weeks (w), birth weight (BW) <1,250 g (g)] were analyzed. IFN-γ was measured in a subgroup of 38 infants by using a biochip multi-analyte immunoassay. The level of IP-10 was determined using a commercially available ELISA kit. Total protein in TA was measured by Bradford assay to correct for sampling related dilution. BPD was defined as the need of supplemental oxygen at 36 weeks postmenstrual age (PMA).

RESULTS:

Twenty infants (GA 26.4 ± 1.9w, BW 860 ± 201 g) survived without BPD at 36 weeks PMA and 59 infants (GA 25.5 ± 1.5w, BW 751 ± 163 g) died before 36 weeks PMA or developed BPD. The mean IFN-γ level was higher in infants who died or developed BPD (9.7 ± 2.8 vs. 3.1 ± 1.1 pg/ml, P = 0.03). Similarly, the mean IP-10 level was higher in infants who died or developed BPD (63.4 ± 17.5 pg/ml) compared to those who survived without BPD (18.5 ± 7.5 pg/ml, P = 0.02).

CONCLUSIONS:

Higher IFN-γ and IP-10 levels in TA samples are associated with the development of BPD or death in premature infants.

PMID:
22431160
DOI:
10.1002/ppul.22540
[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Wiley
    Loading ...
    Support Center