Elevated plasma long pentraxin-3 levels and primary graft dysfunction after lung transplantation for idiopathic pulmonary fibrosis.

Elevated plasma long pentraxin-3 levels and primary graft dysfunction after lung transplantation for idiopathic pulmonary fibrosis.
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DOI:
10.1111/j.1600-6143.2011.03702.x
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发表时间:
2011-11
期刊:
American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons
影响因子:
--
通讯作者:
Lung Transplant Outcomes Group
Lung Transplant Outcomes Group
中科院分区:
其他
文献类型:
--
作者:
Diamond JM;Lederer DJ;Kawut SM;Lee J;Ahya VN;Bellamy S;Palmer SM;Lama VN;Bhorade S;Crespo M;Demissie E;Sonett J;Wille K;Orens J;Shah PD;Weinacker A;Weill D;Kohl BA;Deutschman CC;Arcasoy S;Shah AS;Belperio JA;Wilkes D;Reynolds JM;Ware LB;Christie JD;Lung Transplant Outcomes Group

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肺移植术后原发性移植物功能障碍(PGD)可能是由缺血再灌注损伤(IRI)引起的。对IRI的天然免疫应答可能通过Toll样受体和IL-1诱导的长五聚蛋白-3(PTX-3)释放介导。我们假设PTX 3水平升高与PGD相关。我们对来自肺移植结局组队列的特发性肺纤维化(IPF)或慢性阻塞性肺疾病(COPD)肺移植受者进行了巢式病例对照研究。在移植前以及再灌注后6小时和24小时测量PTX 3水平。病例为移植后72年内发生3级PGD的受试者,对照组为未发生3级PGD的受试者。采用广义估计方程和多因素Logistic回归进行分析。我们选择了40例PGD病例和79例非PGD对照。血浆PTX 3水平与IPF患者的PGD相关,但与COPD患者无关(相互作用p <0.03)。在IPF患者中,6小时和24小时的PTX 3水平与PGD相关(6小时OR=1.6,p=0.02; 24小时OR=1.4,p=0.008)。PTX 3水平升高与IPF患者肺移植后PGD的发生相关。需要进一步研究评估先天免疫激活在IPF和PGD中的作用。
Primary graft dysfunction (PGD) after lung transplantation may result from ischemia-reperfusion injury (IRI). The innate immune response to IRI may be mediated by Toll-like receptor and IL-1-induced long pentraxin-3 (PTX3) release. We hypothesized that elevated PTX3 levels were associated with PGD. We performed a nested case control study of lung transplant recipients with Idiopathic Pulmonary Fibrosis (IPF) or Chronic Obstructive Pulmonary Disease (COPD) from the Lung Transplant Outcomes Group cohort. PTX3 levels were measured pre-transplant, and 6 and 24 hours post reperfusion. Cases were subjects with grade 3 PGD within 72 of transplantation and controls were those without grade 3 PGD. Generalized estimating equations and multivariable logistic regression was used for analysis. We selected 40 PGD cases and 79 non-PGD controls. Plasma PTX3 level was associated with PGD in IPF but not COPD recipients (p for interaction<0.03). Among patients with IPF, PTX3 levels at 6 and 24 hours were associated with PGD (OR=1.6, p=0.02 at 6hrs; OR=1.4, p=0.008 at 24hrs). Elevated PTX3 levels were associated with the development of PGD after lung transplantation in IPF patients. Future studies evaluating the role of innate immune activation in IPF and PGD are warranted.
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