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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.

Human cutaneous leishmaniasis: ultrastructural interactions between the inflammatory cells and leishman bodies in the skin lesions