Houghton J M, Korah R M, Kim K H, Small M B
Department of Medicine (Division of Gastroenterology), University of Medicine and Dentistry of New Jersey-New Jersey Medical School, Newark 07103, USA.
J Infect Dis. 1997 May;175(5):1216-9. doi: 10.1086/593671.
Lack of understanding of the mechanism of tissue destruction associated with idiopathic esophageal ulcers (IEUs) poses a diagnostic and therapeutic dilemma for the clinician. The possible role of apoptosis in IEUs, as suggested by endoscopic and histologic observations, was investigated by examination of archival tissues for apoptosis-related DNA fragmentation using in situ nick end labeling (TUNEL). High levels of apoptosis were observed in mucosal cells immediately adjacent to IEUs. Apoptotic cells were virtually absent in normal control tissues, while the edges and bases of lesions and sloughed-off tissues in IEUs in human immunodeficiency virus (HIV)-infected patients showed elevated levels of apoptotic cell death. However, tissue samples from patients with esophageal ulcerations of known etiology showed no apoptosis of mucosal cells. These data support a role for apoptosis in the pathogenesis of IEUs and suggest a mechanism involving HIV-associated bystander killing of uninfected mucosal cells.
对与特发性食管溃疡（IEU）相关的组织破坏机制缺乏了解，给临床医生带来了诊断和治疗上的两难困境。根据内镜和组织学观察结果推测，凋亡在IEU中可能发挥的作用，通过使用原位缺口末端标记法（TUNEL）检测存档组织中与凋亡相关的DNA片段化进行了研究。在紧邻IEU的黏膜细胞中观察到高水平的凋亡。正常对照组织中几乎不存在凋亡细胞，而在人类免疫缺陷病毒（HIV）感染患者的IEU中，病变的边缘和底部以及脱落组织显示凋亡细胞死亡水平升高。然而，已知病因的食管溃疡患者的组织样本未显示黏膜细胞凋亡。这些数据支持凋亡在IEU发病机制中发挥作用，并提示一种涉及HIV相关的未感染黏膜细胞旁观者杀伤的机制。
