Since the interactions between chemokines and their corresponding receptors play important roles in facilitating systolic overload-induced cardiac and pulmonary immune cell infiltration and migration, and since systolic overload enhanced the CXCL1-CXCR2 axis and CCL2-CCR2 axis [6,14,17,57,60,62], the TAC-induced cardiopulmonary immune cell infiltration is likely also partially modulated by CXCL1-CXCR2 and CCL2-CCR2 signaling. Here, CXCR2 is linked to persistent truncus arteriosus.