Komar Hannah M, Hart Phil A, Cruz-Monserrate Zobeida, Conwell Darwin L, Lesinski Gregory B
From the *Comprehensive Cancer Center, The Arthur G. James Cancer Hospital and Richard J. Solove Research Institute; †Division of Gastroenterology, Hepatology, and Nutrition; ‡Comprehensive Cancer Center, The Arthur G. James Cancer Hospital and Richard J. Solove Research Institute and the Division of Gastroenterology, Hepatology, and Nutrition; §Division of Gastroenterology, Hepatology, and Nutrition, The Ohio State University Wexner Medical Center, Columbus, OH; and ∥Department of Hematology and Oncology, Winship Cancer Institute of Emory University, Atlanta, GA.
Pancreas. 2017 Sep;46(8):986-993. doi: 10.1097/MPA.0000000000000896.
Inflammatory and fibrotic events that drive chronic pancreatitis (CP) are likely orchestrated via signaling of soluble cytokines and chemokines systemically and within the pancreas. However, a comprehensive summary of the expression of such factors during CP has not been reported to date. This information is important given continued interest in targeting cytokines that influence CP pathogenesis. Reported data on the expression change of soluble immunomodulatory factors in human CP patients were identified via a literature search using a single search term. Thirty-one articles meeting the prespecified inclusion criteria were identified to generate a compiled data summary. Compiled data demonstrated up-regulation of several factors in the blood or pancreas microenvironment of CP patients. Nine factors were elevated in both compartments, including fractalkine, IFN-γ, interleukin 1β, IL-6, IL-8, macrophage inhibitory cytokine 1, neutrophil gelatinase-associated lipocalin, transforming growth factor β, and tumor necrosis factor α. Most up-regulated factors could be classified into one of several functional groups, including inflammation, chemotaxis, angiogenesis, bone remodeling, extracellular matrix remodeling, and pain. After further validation, these factors may be used as biomarkers for disease diagnosis and identification of comorbidities, or as potential therapeutic targets.
驱动慢性胰腺炎(CP)的炎症和纤维化事件可能是通过可溶性细胞因子和趋化因子在全身及胰腺内的信号传导来协调的。然而,迄今为止尚未有关于CP期间这些因子表达的全面总结报道。鉴于对影响CP发病机制的细胞因子的持续关注,这一信息很重要。通过使用单一搜索词进行文献检索,确定了关于人类CP患者可溶性免疫调节因子表达变化的报道数据。共识别出31篇符合预定纳入标准的文章,以生成汇总数据总结。汇总数据表明,CP患者血液或胰腺微环境中的几种因子上调。有9种因子在两个部位均升高,包括 fractalkine、IFN-γ、白细胞介素1β、IL-6、IL-8、巨噬细胞抑制细胞因子1、中性粒细胞明胶酶相关脂质运载蛋白、转化生长因子β和肿瘤坏死因子α。大多数上调因子可归类为几个功能组之一,包括炎症、趋化性、血管生成、骨重塑、细胞外基质重塑和疼痛。经过进一步验证后,这些因子可作为疾病诊断和合并症识别的生物标志物,或作为潜在的治疗靶点。