We demonstrated that LPAR1-deficiency reduces the influx of inflammatory cells and IL-6 after a LPS challenge in adult rats and, more effectively, the second hit response against LPS in adult rats with neonatal chronic lung disease or BPD, in which not only the influx of inflammatory cells and IL-6 was strongly reduced, but also the mRNA expression of IL-6, MCP-1, CINC1, TF, and PAI-1. Here, LPAR1 is linked to bronchopulmonary dysplasia.