Chen Tianyi, Liu Jiachen, Hang Ruyi, Chen Qian, Wang Dong
Cancer Center, Daping Hospital, Army Medical University, Chongqing, People's Republic of China.
Radiology Department, Daping Hospital, Army Medical University, Chongqing, People's Republic of China.
J Inflamm Res. 2025 Jan 22;18:925-947. doi: 10.2147/JIR.S497701. eCollection 2025.
Inflammatory bowel disease (IBD) is a non-specific inflammatory disease of digestive tract, primarily manifesting as ulcerative colitis (UC) and Crohn's disease (CD). The precise etiology of IBD remains elusive. The interplay of genetic factors, environmental influences, and intestinal microbiota contributes to the establishment of an uncontrolled immune environment within the intestine, which can progressively lead to atypical hyperplasia and ultimately to malignancy over a long period. This colorectal malignant tumor that arises from chronic IBD is referred to as colitis-associated colorectal cancer (CAC). Dysregulation in the quantity and functionality of neutrophils plays a significant role in the onset, progression, and recurrence of IBD, as well as in the transition from IBD to CAC. Neutrophils affect the pathophysiology of IBD through various mechanisms, including the production of reactive oxygen species (ROS), degranulation, the release of inflammatory mediators and chemokines, and the formation of neutrophil extracellular traps (NETs). These processes can induce DNA mutations, thereby facilitating the development of colon cancer. Given the incomplete understanding of the disease mechanisms underlying IBD and CAC, effective treatment and prevention strategies remain challenging. Consequently, a comprehensive review of the functional roles of neutrophils in IBD and CAC is essential for advancing our understanding of IBD pathogenesis and identifying potential therapeutic targets.
炎症性肠病（IBD）是一种消化道非特异性炎症性疾病，主要表现为溃疡性结肠炎（UC）和克罗恩病（CD）。IBD的确切病因仍不清楚。遗传因素、环境影响和肠道微生物群的相互作用导致肠道内形成失控的免疫环境，长期来看，这可能逐渐导致非典型增生并最终发展为恶性肿瘤。这种由慢性IBD引发的结直肠恶性肿瘤被称为结肠炎相关结直肠癌（CAC）。中性粒细胞数量和功能的失调在IBD的发病、进展和复发以及从IBD向CAC的转变中起重要作用。中性粒细胞通过多种机制影响IBD的病理生理学，包括活性氧（ROS）的产生、脱颗粒、炎症介质和趋化因子的释放以及中性粒细胞胞外陷阱（NETs）的形成。这些过程可诱导DNA突变，从而促进结肠癌的发展。鉴于对IBD和CAC潜在疾病机制的了解尚不完整，有效的治疗和预防策略仍然具有挑战性。因此，全面综述中性粒细胞在IBD和CAC中的功能作用对于增进我们对IBD发病机制的理解以及确定潜在治疗靶点至关重要。
