A case of conventional treatment failure in visceral leishmaniasis: leukocyte distribution and cytokine expression in splenic compartments

dos-Santos, Washington L. C.; Pagliari, Carla; Santos, Lina Gomes dos; Almeida, Valter dos Anjos; Silva, Thiago L V e; Coutinho, João de J; Souza, Túlio Geraldo de Souza e; Duarte, Maria Irma Seixas; Freitas, Luiz Antônio Rodrigues de; Costa, Carlos Henrique Nery

doi:10.1186/1471-2334-14-491

Cited by 14 publications

(11 citation statements)

References 11 publications

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“…Amphotericin B, particularly in liposomal formulation ( 84 ), has become the drug of choice in developed countries and where antimony resistance is problematic; but issues of cost and toxicity remain. Also, there are already clinical cases of treatment failure related to liposomal amphotericin B ( 67 , 85 ). The onset of immunosuppression is a critical event during the progression of VL in a susceptible population.…”

Section: Discussionmentioning

confidence: 99%

“…A new approach to develop treatment strategy against VL in resistance cases has to take into account not only by the development of new leishmanicidal drugs but also by the drugs that could reverse the anergic immune response and pathophysiological changes during VL, such as hypocholesterolemia and splenic neovascularization. The use of an anti-vascular therapy (with Sm, for instance) could be an alternative choice to splenectomy in cases of failure treatment for lipossomal Amphotericin B ( 67 , 85 ).…”

Section: Discussionmentioning

confidence: 99%

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The Contribution of Immune Evasive Mechanisms to Parasite Persistence in Visceral Leishmaniasis

et al. 2016

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Leishmania is a genus of protozoan parasites that give rise to a range of diseases called Leishmaniasis that affects annually an estimated 1.3 million people from 88 countries. Leishmania donovani and Leishmania (L.) infantum chagasi are responsible to cause the visceral leishmaniasis. The parasite can use assorted strategies to interfere with the host homeostasis to establish persistent infections that without treatment can be lethal. In this review, we highlight the mechanisms involved in the parasite subversion of the host protective immune response and how alterations of host tissue physiology and vascular remodeling during VL could affect the organ-specific immunity against Leishmania parasites.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

The Contribution of Immune Evasive Mechanisms to Parasite Persistence in Visceral Leishmaniasis

et al. 2016

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“…The most evident change is spleen enlargement. In humans, the spleen may reach the right lower quadrant of the abdomen and gives rise to hypersplenism, a syndrome characterized by anemia, thrombocytopenia and low white blood cell counts (Dos-Santos et al, 2014 ). In fact, a decrease in spleen size is used as a parameter of therapeutic response in human VL (Kip et al, 2015 ).…”

Section: Spleen Disorganization In Vlmentioning

confidence: 99%

Histological Disorganization of Spleen Compartments and Severe Visceral Leishmaniasis

Hermida

Melo

Lima

et al. 2018

Front. Cell. Infect. Microbiol.

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The spleen is a secondary lymphoid organ responsible for immune surveillance against blood-circulating pathogens. Absence of the spleen is associated with increased susceptibility to systemic spread and fatal infection by different pathogens. Severe forms of visceral leishmaniasis are associated with disorganization of spleen compartments where cell interactions essential for splenic immunological function take place. White pulp atrophies, secondary lymphoid follicles and marginal zones vanish, and the boundaries separating white and red pulp blur. Leukocyte populations are reduced or disappear or are replaced by plasma cells. In this paper, we review the published data on spleen disorganization in severe forms of visceral leishmaniasis and propose a histological classification to help the exchange of information among research groups.

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“…Although the spleen compartments contain the crucial elements to effectively respond to Leishmania infection, in severe cases of disease, the spleen undergoes sequential changes of WP hyperplasia, atrophy and disruption (11). Spleen enlargement leads to hypersplenism syndrome with increased leukocyte and platelet retention and destruction of blood cells (12,13).…”

Section: Introductionmentioning

confidence: 99%

Phenotypical Characterization of Spleen Remodeling in Murine Experimental Visceral Leishmaniasis

et al. 2020

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Background: Visceral leishmaniasis (VL) is caused by Leishmania infantum or L. donovani infection. One of the main problems related to this disease is the emergence of severe clinical forms with a lethality of 5-20%, even while under specific treatment. In humans and other species susceptible to fatal VL, such as dogs and hamsters, the disruption of splenic white pulp (WP) is accompanied by disease progression. Control of VL progression is seen in BALB/c mice, as evidenced by a mild clinical presentation and controlled parasite replication in the liver and spleen. In this study, we investigated the features involved in the morphological remodeling of splenic compartments associated with the control of VL progression to death. Methods: We evaluated cohorts of BALB/c mice after 30, 60, and 90 days of infection by L. infantum. Spleen morphology, cell population subsets and cytokine production were studied in the spleen using flow-and histo-cytometry. Results: Intraperitoneal infection with 10 8 promastigotes of L. infantum led to progressive increases in spleen size at 60 and 90 days after infection. Splenomegaly was the only clinical sign of disease observed. At 30 days after infection, hyperplasia in the WP and decreased numbers of plasmacytoid dendritic cells were observed. The WP hyperplasia subsided at 60 days post-infection. However, the splenomegaly remained in association with increased numbers of macrophages, B and T lymphocytes and plasma cells. An increased number of lymphoid tissue inducer (LTi) cells was observed; these were distributed around the periarteriolar lymphoid sheath in control mice and scattered throughout the red pulp in the Leishmania-infected mice. After 90 days of infection, increased IL-6 and IFN-γ production was seen in the spleen, as well as higher frequencies of follicular and plasmacytoid dendritic cells. Conclusion: The data presented herein emphasizes the potential role of spleen remodeling in the control of severe forms of VL and highlights features potentially involved in this process.

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A case of conventional treatment failure in visceral leishmaniasis: leukocyte distribution and cytokine expression in splenic compartments

Cited by 14 publications

References 11 publications

The Contribution of Immune Evasive Mechanisms to Parasite Persistence in Visceral Leishmaniasis

The Contribution of Immune Evasive Mechanisms to Parasite Persistence in Visceral Leishmaniasis

Histological Disorganization of Spleen Compartments and Severe Visceral Leishmaniasis

Phenotypical Characterization of Spleen Remodeling in Murine Experimental Visceral Leishmaniasis

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