Elevated visfatin levels illuminate the inflammatory path in bronchopulmonary dysplasia

Bronchopulmonary dysplasia (BPD) is a chronic lung disease in premature infants caused by an imbalance between lung injury and lung repair in the developing immature lungs of the newborn. Pulmonary inflammation is an important feature in the pathogenesis of BPD. The aim of this study was to evaluate the relationship between the inflammatory microenvironment and the levels of visfatin and nesfatin-1, which are among the new adipocytokines, in BPD patients.

The groups consisted of 30 patients with BPD and 30 healthy children. Plasma levels of visfatin and nesfatin-1 and inflammation-related markers including interleukin-4 (IL-4), interleukin-10 (IL-10), nuclear factor kappa B (Nf-κB) and matrix metalloproteinase-9 (MMP-9) were determined by enzyme-linked immunosorbent assay (ELISA). RT-PCR was performed to evaluate the change in mRNA expression of visfatin and nesfatin-1 in the groups.

Visfatin levels were significantly higher in the BPD group compared to the healthy control (7.05±4.07 ng/ml vs. 2.13±1.66 ng/ml, p<0.0001). There was a 1.36±0.12 fold increase in visfatin mRNA expression (p<0.05) in the BPD group. There was no significant difference in plasma levels of nesfatin-1, IL-4, and IL-10 between the groups. Although MMP-9 and Nf-κB levels were significantly higher in the BPD group (p<0.0001), there was no correlation between visfatin levels and MMP-9 and Nf-κB levels in BPD patients.

This study showed that significant changes in visfatin levels in BPD patients might be associated with the risk of developing inflammation in BPD.