el-Shoura S M, Tallab T, Bahamdan K
Department of Pathology, College of Medicine, King Saud University, Abha, Kingdom of Saudi Arabia.
Parasite. 1996 Sep;3(3):229-36. doi: 10.1051/parasite/1996033229.
The ultrastructural interactions between the inflammatory infiltrate and Leishman bodies (LBs) were described in skin lesions from 16 patients with acute cutaneous leishmaniasis. In early stages of the inflammation, the cellular infiltrate consisted of both undifferentiated and differentiated (activated) monocytes (M), macrophages (Mc), multinucleated giant cells (MNGC), plasma cells (PC), lymphocytes (Ly), and fibroblasts (F). In late stages, the infiltrate was in the form of tuberculous granulomas consisted mainly of type I secretory, and type II vesicular epithelioid cells (ECs), in addition to remnant of some inflammatory cells seen in the early stages. The two types of ECs were found only in six patients. The activated M, Mc and MNGC were often parasitized by LBs. The parasites were enclosed within the host cell digestive vacuoles (DVs), or phagolysosomes, together with skin melanosomes which are known to have lysosomal effect. In the DVs, LBs either survived or were killed and expelled from the host cell cytoplasm. This study showed, for the first time, that the melanosomes were apparently involved in killing of the LBs possibly by increasing the fatal effects of the DVs hydrolytic enzymes. Plasma cells were packed with large "Russell's bodies" indicating a high cellular immunoglobulin activity. The large, granular lymphocytes were in close contact to the activated M, possibly to promote delivery of activation signals. The type I secretory ECs contained mucin-like granules with electrondense cores. In late stages of inflammation, the type II vesicular ECs contained lysosomal granules, and were found together with the type I ECs in broken-down tuberculous granulomas. The type I secretory ECs were previously thought to produce a mediator, or "granuloma factor" which recruits undifferentiated mononuclear cells to perpetuate the granulomatous process; while the type II vesicular ECs were thought to appear where the granulomatous process in brought to an end, preceeding the healing by fibrosis.
在16例急性皮肤利什曼病患者的皮肤病变中，对炎症浸润与利什曼小体（LBs）之间的超微结构相互作用进行了描述。在炎症早期，细胞浸润由未分化和分化（活化）的单核细胞（M）、巨噬细胞（Mc）、多核巨细胞（MNGC）、浆细胞（PC）、淋巴细胞（Ly）和成纤维细胞（F）组成。在后期，浸润呈结核样肉芽肿形式，主要由I型分泌性和II型囊泡状上皮样细胞（ECs）组成，此外还有早期可见的一些炎症细胞残余。仅在6例患者中发现了这两种类型的ECs。活化的M、Mc和MNGC常被LBs寄生。寄生虫与已知具有溶酶体作用的皮肤黑素体一起被包裹在宿主细胞消化泡（DVs）或吞噬溶酶体内。在DVs中，LBs要么存活，要么被杀死并从宿主细胞质中排出。本研究首次表明，黑素体显然参与了LBs的杀伤，可能是通过增强DVs水解酶的致命作用。浆细胞充满了大的“拉塞尔小体”，表明细胞免疫球蛋白活性很高。大的颗粒淋巴细胞与活化的M紧密接触，可能是为了促进激活信号的传递。I型分泌性ECs含有带电子致密核心的粘蛋白样颗粒。在炎症后期，II型囊泡状ECs含有溶酶体颗粒，并在分解的结核样肉芽肿中与I型ECs一起被发现。I型分泌性ECs以前被认为产生一种介质或“肉芽肿因子”，可招募未分化的单核细胞以使肉芽肿过程持续；而II型囊泡状ECs被认为出现在肉芽肿过程结束的地方，在纤维化愈合之前。
