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Ann Thorac Surg 2006;81:1844-1850
© 2006 The Society of Thoracic Surgeons

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Original article: General thoracic

Cytokine Profile After Lung Transplantation: Correlation With Allograft Injury

^a Department of Surgery, Division of Thoracic and Cardiovascular Surgery, University of Florida, Gainesville, Florida
^b Department of Medicine, Division of Pulmonology, University of Florida, Gainesville, Florida
^c Department of Radiology, Division of Thoracic Radiology, University of Florida, Gainesville, Florida
^d Department of Surgery, Laboratory of Inflammation Biology and Surgical Science, University of Florida, Gainesville, Florida

Accepted for publication November 28, 2005.

^_* Address correspondence to Dr Beaver, Division of Thoracic and Cardiovascular Surgery, PO Box 100286, Gainesville, FL 32610-0286 (Email: beavetm{at}surgery.ufl.edu).

Presented at the Forty-first Annual Meeting of The Society of Thoracic Surgeons, Tampa, FL, Jan 24–26, 2005.

BACKGROUND: Post–lung transplant reperfusion edema (PLTRE) and its more severe form, primary graft failure (PGF), occur in 10% to 60% of lung transplant recipients. We hypothesized that PLTRE and PGF would be associated with an elevated proinflammatory cascade and that the allograft would be the source of cytokine appearance in the circulation.

METHODS: Pulmonary arterial and systemic arterial samples were obtained at baseline and at 4, 8, and 24 hours after reperfusion. Post–lung transplant reperfusion-edema and PGF were defined as PaO₂/FiO₂ less than 300 with a mild or moderate infiltrate, or less than 200 with a severe infiltrate and ventilator dependence after 72 hours, respectively. Tumor necrosis factor alpha (TNF), interleukin (IL)-6, IL-8, and IL-10 concentrations were determined by immunoassay.

RESULTS: Fifteen single and 6 bilateral lung recipients were studied. Six (29%) had PLTRE and 4 (19%) had PGF; these patients had an overall elevation in plasma IL-6, IL-8, and IL-10 concentrations (all p < 0.05). Subgroup analysis revealed a significantly greater elevation in IL-6, IL-8, and IL-10 levels in PGF patients (all p < 0.01) versus PLTRE. In the PGF group, TNF and IL-10 concentrations were significantly greater in the systemic versus the pulmonary arterial samples (p < 0.05).

CONCLUSIONS: Patients with PLTRE and PGF exhibited graded increases in IL-6, IL-8, and IL-10 concentrations. The PGF patients had higher TNF and IL-10 systemic arterial concentrations overall, consistent with the allograft being a source of this cytokine production.

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