Disciplinary Program, Institute of Biomedical Sciences, School of Medicine, University of Chile, Independencia 1027, 8380453 Santiago, Chile.
Department of Immunology, School of Medicine, Siriraj Hospital, Mahidol University, 2 Prannok Road, Bangkok Noi, Bangkok 10700, Thailand.
J Immunol Res. 2014;2014:149185. doi: 10.1155/2014/149185. Epub 2014 May 13.
Acute inflammation is a response to an alteration induced by a pathogen or a physical or chemical insult, which functions to eliminate the source of the damage and restore homeostasis to the affected tissue. However, chronic inflammation triggers cellular events that can promote malignant transformation of cells and carcinogenesis. Several inflammatory mediators, such as TNF-α, IL-6, TGF-β, and IL-10, have been shown to participate in both the initiation and progression of cancer. In this review, we explore the role of these cytokines in important events of carcinogenesis, such as their capacity to generate reactive oxygen and nitrogen species, their potential mutagenic effect, and their involvement in mechanisms for epithelial mesenchymal transition, angiogenesis, and metastasis. Finally, we will provide an in-depth analysis of the participation of these cytokines in two types of cancer attributable to chronic inflammatory disease: colitis-associated colorectal cancer and cholangiocarcinoma.
急性炎症是对病原体或物理化学损伤引起的变化的反应，其功能是消除损伤源并使受影响的组织恢复到体内平衡。然而，慢性炎症会引发细胞事件，从而促进细胞的恶性转化和癌变。已经证实，几种炎症介质，如 TNF-α、IL-6、TGF-β 和 IL-10，参与了癌症的发生和发展。在这篇综述中，我们探讨了这些细胞因子在致癌作用的重要事件中的作用，例如它们产生活性氧和氮物种的能力、潜在的诱变作用以及它们在上皮间质转化、血管生成和转移机制中的参与。最后，我们将深入分析这些细胞因子在两种由慢性炎症性疾病引起的癌症中的参与情况：结肠炎相关结直肠癌和胆管癌。
