Department of Surgery, University of Alberta, Alberta, Canada.
Curr Opin Infect Dis. 2010 Jun;23(3):259-67. doi: 10.1097/QCO.0b013e32833939cb.
The present review summarizes key studies on the effects of major abdominal surgery on the host response to infection published during the last 18 months.
Surgical trauma causes stereotyped systemic proinflammatory and compensatory anti-inflammatory reactions. It is leukocyte reprogramming rather than general immune suppression. The list of recent findings is long. Preoperative infectious challenge was found to increase survival. Obesity is associated with increased production of interleukin-17A in peritonitis. Abdominal surgery alters expression of toll-like receptors (TLRs). The acute phase reaction down-regulates the transcription factor carbohydrate response element binding protein. Myosin light chain kinase activation is a final pathway of acute tight junction regulation of gut barrier and zonula occludens 1 protein is an essential effector. The brain is involved in regulating the immune and gut system. Elimination of lipopolysaccharide is challenging. Th1/Th2 ratio is lowered in patients with postoperative complications. Cholinergic anti-inflammatory pathways can inhibit tissue damage. The new substance PXL01 prevents adhesions. Postoperative infection causes incisional hernias. Hypothermia reduced human leukocyte antigen DR surface expression and delayed tumor necrosis factor clearance. Systems biology identified interferon regulatory factor 3 as the negative regulator of TLR signaling. Protective immunity could contribute defeating surgical infections.
Systemic inflammation is the usual response to trauma. All organs seem to be involved and linked up in cybernetic systems aiming at reconstitution of homeostasis. Although knowledge is still fragmentary, it is already difficult to integrate known facts and new technologies are required for information processing. Defining criteria to develop therapeutic strategies requires much more insight into molecular mechanisms and cybernetics of organ systems.
本文总结了过去 18 个月中关于主要腹部手术后宿主对感染反应的关键研究。
手术创伤引起典型的全身促炎和代偿性抗炎反应。这是白细胞重编程，而不是普遍的免疫抑制。最近的发现很多。术前感染性挑战被发现可提高生存率。肥胖与腹膜炎中白细胞介素-17A 的产生增加有关。腹部手术改变了 Toll 样受体（TLR）的表达。急性期反应下调转录因子碳水化合物反应元件结合蛋白。肌球蛋白轻链激酶的激活是肠道屏障紧密连接调节的终末途径，闭合蛋白 1 是必需的效应蛋白。大脑参与调节免疫和肠道系统。清除脂多糖具有挑战性。术后并发症患者的 Th1/Th2 比值降低。胆碱能抗炎途径可抑制组织损伤。新物质 PXL01 可预防粘连。术后感染导致切口疝。低温减少人类白细胞抗原 DR 表面表达并延迟肿瘤坏死因子清除。系统生物学发现干扰素调节因子 3 是 TLR 信号的负调节剂。保护性免疫可能有助于抵御手术感染。
全身炎症是创伤的常见反应。所有器官似乎都参与其中，并在旨在重建体内平衡的控制系统中相互关联。尽管知识仍然是零碎的，但已经很难整合已知事实，需要新的技术来进行信息处理。定义开发治疗策略的标准需要对器官系统的分子机制和控制系统有更深入的了解。
