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

Abstract

Leishmania spp. (Kinetoplastida) are unicellular parasites causing leishmaniases, neglected tropical diseases of medical and veterinary importance. In the vertebrate host, Leishmania parasites multiply intracellularly in professional phagocytes, such as monocytes and macrophages. However, their close relative with intracellular development—Trypanosoma cruzi—can unlock even non-professional phagocytes. Since Leishmania and T. cruzi have similar organelle equipment, is it possible that Leishmania can invade and even proliferate in cells other than the professional phagocytes? Additionally, could these cells play a role in the long-term persistence of Leishmania in the host, even in cured individuals? In this review, we provide (i) an overview of non-canonical Leishmania host cells and (ii) an insight into the strategies that Leishmania may use to enter them. Many studies point to fibroblasts as already established host cells that are important in latent leishmaniasis and disease epidemiology, as they support Leishmania transformation into amastigotes and even their multiplication. To invade them, Leishmania causes damage to their plasma membrane and exploits the subsequent repair mechanism via lysosome-triggered endocytosis. Unrevealing the interactions between Leishmania and its non-canonical host cells may shed light on the persistence of these parasites in vertebrate hosts, a way to control latent leishmaniasis.

Proteome profiling of cutaneous leishmaniasis lesions due to dermotropicLeishmania donovaniin Sri Lanka

“…Tandem mass spectrometry was performed using ion trap mode to ensure the highest signal intensity of MS 2 spectra using both collision-induced dissociation (CID) for 2+ and 3+ charges and electrontransfer dissociation (ETD) for 4+ to 6+ charges. The AGC target ion number for the ion trap MS 2 scan was set at 1000 ions, the maximum ion injection time was set at 100 ms, and micro scan number was set at 1. The CID fragmentation energy was set to 35%.…”

Revolutionizing Leishmaniasis Treatment with Cutting Edge Drug Delivery Systems and Nanovaccines: An Updated Review

“…Phagocytosis is an endocytosis process in which particles bigger than 0.75 nm are engulfed by the macrophages; this is how these drug-loaded nanocarriers enter inside the cells. , Macrophages, neutrophils, and monocytes are frequently called “professional phagocytes” because of their ability to phagocytose (Figure ). Since the parasites responsible for leishmaniasis infect not only macrophages but also fibroblasts, adipocytes or adipose-tissue mesenchymal stem cells, and neutrophils, a highly phagocytic cell, this illness provides a unique opportunity for drug-loaded nanocarriers to treat the disease. The drug-loaded nanocarrier is ingested by the macrophages via phagocytosis and then is used to destroy the parasites.…”

Elucidating the role played by bone marrow in visceral leishmaniasis

“…As stem cells tend to remain quiescent in the absence of an external stimulus, this suggests that they may also serve as an ideal host cell reservoir for Leishmania ( Allahverdiyev et al., 2011 ). While the mechanism by which Leishmania invades MSCs has yet to be fully elucidated, it has been reported that the MSCs found in adipose tissue possess phagocytic properties ( Valigurová and Kolářová, 2023 ).…”

“…Regarding parasite persistence in organs such as the bone marrow, the discontinuation of primary VL treatment regimens was hypothesized as a model capable of elucidating associations between therapeutic failure and disease relapse ( Valigurová and Kolářová, 2023 ). Recently, Dirkx et al.…”