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

Abstract

Summary :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.KEYWORDS : cutaneous leishmaniasis, human, cellular infiltrate, inflammation, ultrastructure.MOTS CLES : leishmaniose cutanée, homme, infiltrat cellulaire, inflammation, ultrastructure. Résumé : LEISHMANIOSE CUTANÉE HUMAINE : INTERACTIONS ENTRE INFILTRAT INFLAMMATOIRE ET CORPS DE LEISHMAN DANS LES LÉSIONS CUTANÉES Les interactions entre infiltrat inflammatoire et corps de Leishman (LBs) sont décrites en microscopie électronique dans les lésions cutanées de 16 malades atteints de leishmaniose cutanée aiguë. Dans les premiers stades de l'inflammation, l'infiltrat cellulaire consiste à la fois en monocytes indifférenciés et différenciés (Mj, en macrophages (Mc), en cellules géantes multinuclées (MNGC), en plasmocytes (PC), en lymphocytes (Ly) et en fibroblastes (F). Dans les stades avancés, l'infiltrat est sous forme de granulomes tuberculeux consistant en cellules épithélioides de type I secrétoire et de type II vésiculaire (ECs), en plus de quelques cellules Inflammatoires observées au cours des premiers stad...

In vivo Confocal Microscopy Features of Cutaneous Leishmaniasis

“…The infiltrate is composed predominantly of macrophages with a mixture of lymphocytes and multinucleated giant cells. Plasma cells may be found in variable amounts and may contain eosinophilic ‘Russel bodies' indicating immunoglobulin production [7]. Neutrophils and eosinophils are present in variable amounts but are usually few in number.…”

Unrevealing the Mystery of Latent Leishmaniasis: What Cells Can Host Leishmania?

“…The most studied non-canonical Leishmania host cells are fibroblasts [ 8 , 9 , 10 , 11 , 12 , 13 , 14 , 15 , 81 , 82 , 83 , 84 , 85 , 86 , 87 , 88 , 89 , 90 , 91 , 92 , 93 , 94 , 95 , 96 ]. They can migrate within the skin tissue [ 8 ], potentially allowing Leishmania to spread from the site of transmission, thereby disseminating the infection and enhancing the possibility of being engulfed by the vector during blood feeding.…”

“…Several in vitro and in vivo studies have reported that fibroblasts harbour Leishmania amastigotes ( Table 1 ) [ 8 , 9 , 10 , 11 , 14 , 81 , 83 , 84 , 85 , 86 , 87 ]. Conflicting results have been observed regarding the survival of L. amazonensis in fibroblasts, ranging from limited survival of parasites (e.g., [ 12 , 91 ]) to their successful multiplication [ 8 , 10 , 14 , 15 ] ( Table 1 ).…”