CINC is the rat homolog of IL-8 which has previously been shown to be increased in the tracheal aspirates of premature babies who later develop bronchopulmonary dysplasia (BPD). Treatment with anti-CINC has ameliorated acute lung injury in endotoxin treated rats. In order to evaluate the potential role of this cytokine class in the development of BPD we sought to evaluate the effects of hyperoxia on CINC expression in a newly developed rat model of BPD (Chen et al., J.Pediatr 1997;130:409). Rats were delivered at gestation day (d)21 (term - 1) and randomly assigned air or 95% oxygen (HO), being reared by just delivered surrogate mother rats. At 4, 6, and 8 days of exposure, rats were killed and lungs were removed for CINC and CINC mRNA analysis. Some lungs were flash frozen for RNA analysis, others were fixed in buffered formalin. CINC mRNA was evaluated by semiquantitative RT-PCR of 2 μg total lung RNA from 4 pups at 4, 6, and 8 d, air or HO exposure, using 32 P dATP incorporation into cDNA products. At 8 d of HO CINC mRNA was over twice the amount detected at 4 d air, p <.01. There was no significant change in CINC mRNA with increasing age in the air exposed group. GAPDH mRNA which is believed to be constitutively expressed, showed no significant change regardless of age or exposure. In situ mRNA hybridization using anti-sense digoxigenin labeled cRNA was done on paraffin sections of HO exposed newborn rat lung and demonstrated increased label intensity in alveolar and bronchiolar epithelium with increasing HO exposure duration. Sections were also labeled with goat anti-rat CINC 1:1000 and demonstrated increased apical staining intensity in bronchiolar epithelium in the 8 d HO exposed pups. Conclusions: HO in prematurely delivered rats increases CINC expression. Increased CINC expression may play a role in neutrophil recruitment in the development of BPD.