Winfield Robert D, Delano Matthew J, Pande Kalyan, Scumpia Philip O, Laface Drake, Moldawer Lyle L
Department of Surgery, University of Florida College of Medicine, Gainesville, FL 32610-0286, USA.
JPEN J Parenter Enteral Nutr. 2008 Nov-Dec;32(6):651-5. doi: 10.1177/0148607108325075.
Cachexia accompanies many chronic inflammatory diseases, including cancer. Lean tissue wasting is only one component of the cancer cachexia response, which also includes anemia, anorexia, a hepatic acute phase protein response, and increased susceptibility to secondary infections. The etiologies of cancer cachexia are multifactorial and include an overproduction of inflammatory mediators, including cytokines produced by inappropriate activation of innate immunity. However, anticytokine therapies have generally not been seriously considered for cancer cachexia, in large part because of the overlapping activities of several inflammatory cytokines and the inability to prospectively identify the contributions of individual mediators. In contrast, recent evidence has focused on an immature myeloid cell population that expands dramatically in the tumors and secondary lymphoid organs of animals with some actively growing tumors. These immature GR-1(+)CD11b(+) cells are metabolically active and secrete large quantities of inflammatory cytokines and chemokines with the potential to produce cachexia. Their expansion is temporally associated with the development of cachexia. Future studies are required to determine whether therapeutic efforts intended to block the expansion of these cells can prevent the lean tissue wasting that accompanies active tumor growth.
恶病质伴随许多慢性炎症性疾病，包括癌症。瘦组织消耗只是癌症恶病质反应的一个组成部分，该反应还包括贫血、厌食、肝脏急性期蛋白反应以及对继发感染易感性增加。癌症恶病质的病因是多因素的，包括炎症介质过度产生，其中包括先天免疫不适当激活所产生的细胞因子。然而，抗细胞因子疗法一般未被认真考虑用于癌症恶病质，很大程度上是因为几种炎症细胞因子的活性重叠，且无法前瞻性地确定单个介质的作用。相比之下，最近的证据集中在一种未成熟髓样细胞群体上，在患有一些活跃生长肿瘤的动物的肿瘤和二级淋巴器官中，这种细胞群体显著扩增。这些未成熟的GR-1(+)CD11b(+)细胞代谢活跃，分泌大量具有产生恶病质潜力的炎症细胞因子和趋化因子。它们的扩增在时间上与恶病质的发展相关。需要进一步的研究来确定旨在阻止这些细胞扩增的治疗措施是否能够预防伴随活跃肿瘤生长的瘦组织消耗。
