Objective Bronchopulmonary dysplasia (BPD) is caused by persistent inflammation, resulting in abnormalities in lung morphogenesis. Wnt5a, a non-canonical Wnt, is expressed in both the mesenchyme and epithelium of the embryonic lung and plays a key role in its morphogenesis. We examined Wnt5a expression by lung inflammatory cells from preterm neonates at risk of BPD.
Methods Inflammatory cells isolated from tracheal aspirates of human preterm neonates were incubated in the presence or absence of lipopolysaccharide and Wnt5a messenger RNA was measured by real-time reverse transcription PCR assay.
Results We studied 18 preterm patients with a mean gestational age of 26.9 weeks, birth weight of 958 g, who were divided into two groups. The first group includes positive responders (Wnt5a increased in samples with lipopolysaccharide over samples without lipopolysaccharide or control, n = 8) and the second group includes negative responders (Wnt5a decreased in samples with lipopolysaccharide over samples without lipopolysaccharide or control, n = 10). Patients with a Wnt5a-positive response to lipopolysaccharide showed a trend towards an inverse relationship with gestational age and birth weight (r = −0.53 and r = −0.51), whereas negative responders showed a trend towards a direct relationship with gestational age and birth weight (r = 0.23 and r = 0.38, respectively). Twenty-five per cent of positive responders and 70% of negative responders had positive blood or tracheal cultures.
Conclusions Our preliminary findings indicate that lung inflammatory cells from preterm neonates constitutively expressed Wnt5a. Expression of Wnt5a may be regulated by inflammation and Wnt5a response to lipopolysaccharide may be related to birth weight and gestational age.
Funding: Supported by NIH and Hastings Foundation.