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Article Abstract
Objectives: Acute lung injury caused by cardiopulmonary bypass (CPB) is characterized by massive neutrophil migration to the lungs. Neutrophil migration may be closely related to stromal cell-derived factor 1 (SDF-1)/C-X-C chemokine receptor Type 4 (CXCR4) axis activation, which plays an essential role in modulating the trafficking of neutrophils. We investigated the changes in the expression of SDF-1/CXCR4 axis components before and after CPB as well as the role of the axis in driving the migration of neutrophils in patients with congenital heart disease.
Methods: Fifteen children undergoing elective open-heart surgery under CPB (CPB group) and 15 children undergoing minimally invasive ultrasound-guided closure of a ventricular septal defect (control group) were enrolled in this non-randomized clinical trial. Neutrophil CXCR4 expression was evaluated using quantitative reverse transcription polymerase chain reaction and flow cytometry. An enzyme-linked immunosorbent assay was used to measure plasma SDF-1 levels. The migration characteristics of neutrophils under 8 different combinations designated A-H were assayed with and without a specific CXCR4 antagonist, AMD3100, to evaluate the functional significance of the SDF-1/CXCR4 axis.
Results: Both CXCR4 gene and protein expressions were elevated in the CPB group compared with the control group after CPB (0.81 ± 0.55 vs 1.76 ± 1.32; P < 0.05, 1.96 ± 0.86 vs 2.65 ± 0.79; P < 0.05), and plasma SDF-1 levels were also increased in the former compared with the latter (197.84 ± 19.96 pg/ml vs 539.13 ± 99.83 pg/ml; P < 0.05). The in vitro experiments showed that plasma isolated post-CPB exhibited the strongest chemotactic effect on neutrophils. The CPB group showed a higher chemotaxis index, which serves as a marker for the effects of plasma on neutrophils, than that for the control group after CPB (37.38 ± 9.39 vs 13.61 ± 2.59; P < 0.05). In addition, the CXCR4 antagonist AMD3100 significantly abrogated the increase in neutrophil migration in the CPB group.
Conclusions: Exposure to CPB, which activates the SDF-1/CXCR4 axis, using an antagonist to prevent neutrophil trafficking, may be a beneficial therapy for the related complications.
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