The beneficial effect of LPAR1-deficiency on the LPS response in rats with BPD is further complicated by the biological response of LPAR1-deficiency on two different injurious stimuli, inflicted at two different time-points, i.e., hyperoxia-induced lung injury in the neonatal period and LPS-exposure during adulthood. Here, LPAR1 is linked to bronchopulmonary dysplasia.