Inflammatory Responses in Liver Transplantation

Q4 Medicine
Kantoku Nagakawa, A. Soyama, S. Eguchi
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引用次数: 0

Abstract

Successful liver transplantation requires proper mitigation of stress responses. Systemic effects caused by liver cirrhosis, invasive surgery, ischemia-reperfusion injury, rejection, and infection, all of which are relevant to liver transplantation, are mediated by inflammatory factors. Recently, the detailed mechanisms of inflammation have been elucidated. Damage-associated molecular patterns (DAMPs) released from cells damaged by ischemia or injury, or pathogen-associated molecular patterns (PAMPs) released by pathogens, are recognized by internal cell receptors or cell surface receptors, leading to the synthesis of inflammatory proteins including proinflammatory/anti-inflammatory cytokines, which are then secreted by the cells. These cytokines stimulate the production of additional cytokines, causing a vicious circle of inflammatory responses, such as innate immune responses by macrophages. In addition, lymphocytes activated by these cytokines stimulate adaptive immunity. During liver transplantation, the general preoperative condition of the patient and surgical invasiveness are associated with organ failure and ischemia-reperfusion injury, which can lead to transplant rejection. It has been suggested that progressive immunodeficiency and organ failure as a result of pre-transplant cirrhosis are associated with postoperative multiple organ failure and death, and that elevated intraoperative DAMPs correlate with organ failure. Furthermore, DAMP receptors and inflammatory cytokines are increased by ischemia-reperfusion injury, indicating its role in promoting innate and adaptive immunity. In addition, inflammatory signals induced by postoperative infections are similar to those induced by ischemia-reperfusion injury and rejection, indicating that pathogen-derived inflammation can also lead to rejection. In summary, most complications in liver transplantation can be explained in a unified manner by abnormal inflammatory responses; therefore, controlling inflammation might be of benefit for the struggle of safe and effective liver transplantation.
肝移植中的炎症反应
成功的肝移植需要适当减轻应激反应。肝硬化、侵袭性手术、缺血再灌注损伤、排斥反应、感染等与肝移植相关的全身性影响均由炎症因子介导。近年来,炎症的详细机制已被阐明。损伤相关分子模式(DAMPs)由缺血或损伤损伤的细胞释放,或病原体释放的病原体相关分子模式(PAMPs)被细胞内部受体或细胞表面受体识别,导致炎症蛋白的合成,包括促炎/抗炎细胞因子,然后由细胞分泌。这些细胞因子刺激其他细胞因子的产生,引起炎症反应的恶性循环,如巨噬细胞的先天免疫反应。此外,被这些细胞因子激活的淋巴细胞刺激适应性免疫。在肝移植过程中,患者的一般术前状况和手术的侵入性与器官衰竭和缺血再灌注损伤有关,这可能导致移植排斥反应。有研究表明,移植前肝硬化导致的进行性免疫缺陷和器官衰竭与术后多器官衰竭和死亡有关,术中DAMPs升高与器官衰竭有关。此外,缺血再灌注损伤后,DAMP受体和炎症细胞因子增加,表明其在促进先天免疫和适应性免疫中的作用。此外,术后感染引起的炎症信号与缺血再灌注损伤和排斥反应引起的炎症信号相似,表明病原性炎症也可导致排斥反应。综上所述,大多数肝移植并发症可以统一解释为异常的炎症反应;因此,控制炎症可能有利于争取安全有效的肝移植。
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来源期刊
Surgery, Gastroenterology and Oncology
Surgery, Gastroenterology and Oncology Medicine-Gastroenterology
CiteScore
0.30
自引率
0.00%
发文量
11
期刊介绍: Starting with this issue "Annals of Fundeni Hospital", founded in 1996 as the scientific journal of the prestigious hospital Fundeni becomes "Journal of Translational Medicine and Research" (JTMR), an Journal of the Academy of Medical Sciences of Romania. Therefore, an 18 years old Journal, attested and indexed in Elsevier Bibliographic Databases, Amsterdam and also indexed in SCOPUS, is continuing a tradition of excellence that lasted almost two decades. The new title of the Journal is inspired first of all from the important developments of translational research In Fundeni Clinical Institute and the "C.C Iliescu Institute for Cardio-Vascular Diseases", in parallel with the national and international trend to promote and develop this important area or medical research. Although devoted mainly to translational research, JTMR will continue to promote both basic and clinical research.
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