Leishmania (Viannia) panamensis - induced cutaneous leishmaniasis in susceptible and resistant mouse strains

Goto, Hiro; Rojas, J. I.; Sporrong, L.; Carreira, P. de; Sánchez, C.; A, Orn

doi:10.1590/s0036-46651995000600001

Cited by 11 publications

(8 citation statements)

References 16 publications

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“…In this model, resistance and susceptibility are clearly associated with Th1 and Th2 responses, respectively (9). However, infection of mice with L. panamensis is distinguished from L. major because 10‐ to 100‐fold more parasites are required to induce footpad swelling, and the lesions are strictly confined to the inoculation site in the skin (28). In addition, although C57BL/6 mice are resistant and BALB/c mice are susceptible to infection with L. panamensis (as for L. major infection), susceptibility is not associated with induction of IL‐4, at least during the first week after infection (29).…”

Section: Discussionmentioning

confidence: 99%

Endemically exposed asymptomatic individuals show no increase in the specific Leishmania (Viannia) panamensis‐Th1 immune response in comparison to patients with localized cutaneous leishmaniasis

Trujillo

Robledo

Franco

et al. 2002

Parasite Immunology

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In Colombia, most cases of human cutaneous leishmaniasis are caused by Leishmania (Viannia) panamensis. Interestingly, up to 30% of the exposed population do not suffer from clinical leishmaniasis although it is likely that they are continuously infected with Leishmania parasites. Since it is believed that the induction of efficient Th1 immune responses protects against Leishmania infections both in humans and in animal models, we determined if endemically exposed asymptomatics showed stronger Leishmania-specific Th1 immune responses than patients with active localized cutaneous leishmaniasis (LCL). We found that Montenegro skin test responses were slightly higher among asymptomatic individuals compared to patients suffering from LCL. However, PBMC from patients with LCL showed similar Leishmania-specific proliferative responses compared to PBMC from asymptomatic individuals. Furthermore, PBMC from both groups also secreted similar amounts of IFN-gamma, IL-12p40 and IL-10 after in vitro exposure to L. panamensis. No IL-4 was detected in the supernatants. Taken together our results suggest that lack of LCL development in endemically exposed asymptomatics cannot be explained by stronger systemic anti-Leishmania Th1 immune responses or decreased Th2 responses in these individuals in comparison to individuals who develop LCL. It may be possible that other mechanisms are responsible for resistance to cutaneous leishmaniasis in Colombia in endemically exposed asymptomatics.

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Section: Discussionmentioning

confidence: 99%

Endemically exposed asymptomatic individuals show no increase in the specific Leishmania (Viannia) panamensis‐Th1 immune response in comparison to patients with localized cutaneous leishmaniasis

Trujillo

Robledo

Franco

et al. 2002

Parasite Immunology

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“…In these footpads, there was a well-preserved inflammatory cell population and intact tissue architecture. In the same model, L. panamensis parasites behave like most Leishmania species inducing a non-healing footpad swelling (Rojas et al, 1993; Goto et al, 1995) having the expected cytokine profile of a “losing battle” in the draining lymph nodes. Here, an early induction of IFN-γ and minimally detectable IL-4 at 24 h post infection was followed by a complete reversal 7 days post infection (Guevara-Mendoza et al, 1997).…”

Section: Experimental Animal Models Of MCLmentioning

confidence: 99%

Leishmania RNA virus: when the host pays the toll

Hartley

Ronet

Zangger

et al. 2012

Front. Cell. Inf. Microbio.

126

143

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The presence of an RNA virus in a South American subgenus of the Leishmania parasite, L. (Viannia), was detected several decades ago but its role in leishmanial virulence and metastasis was only recently described. In Leishmania guyanensis, the nucleic acid of Leishmania RNA virus (LRV1) acts as a potent innate immunogen, eliciting a hyper-inflammatory immune response through toll-like receptor 3 (TLR3). The resultant inflammatory cascade has been shown to increase disease severity, parasite persistence, and perhaps even resistance to anti-leishmanial drugs. Curiously, LRVs were found mostly in clinical isolates prone to infectious metastasis in both their human source and experimental animal model, suggesting an association between the viral hyperpathogen and metastatic complications such as mucocutaneous leishmaniasis (MCL). MCL presents as chronic secondary lesions in the mucosa of the mouth and nose, debilitatingly inflamed and notoriously refractory to treatment. Immunologically, this outcome has many of the same hallmarks associated with the reaction to LRV: production of type 1 interferons, bias toward a chronic Th1 inflammatory state and an impaired ability of host cells to eliminate parasites through oxidative stress. More intriguing, is that the risk of developing MCL is found almost exclusively in infections of the L. (Viannia) subtype, further indication that leishmanial metastasis is caused, at least in part, by a parasitic component. LRV present in this subgenus may contribute to the destructive inflammation of metastatic disease either by acting in concert with other intrinsic “metastatic factors” or by independently preying on host TLR3 hypersensitivity. Because LRV amplifies parasite virulence, its presence may provide a unique target for diagnostic and clinical intervention of metastatic leishmaniasis. Taking examples from other members of the Totiviridae virus family, this paper reviews the benefits and costs of endosymbiosis, specifically for the maintenance of LRV infection in Leishmania parasites, which is often at the expense of its human host.

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“…3 A and B). (21,26). We infected susceptible BALB͞c mice with L. (V.) panamensis with or without IGF-I.…”

Section: Analysis Of Specific Binding Of Igf-i Tomentioning

confidence: 99%

Insulin-like growth factor I is a growth-promoting factor forLeishmaniapromastigotes and amastigotes

Goto

Gomes

Corbett

et al. 1998

Proc. Natl. Acad. Sci. U.S.A.

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Leishmaniases are diseases caused by protozoa of the genus Leishmania that affect more than 20 million people in the world. The initial phase of the infection is fundamental for either the progression or control of the disease. The Leishmania parasites are injected in the skin as promastigotes and then, after been phagocytized by the host macrophages, rapidly transform into amastigotes. In this phase different nonspecific cellular and humoral elements participate. We have shown previously that insulin-like growth factor (IGF)-I that is constitutively present in the skin induces growth of Leishmania promastigotes. In the present paper we show further evidence for the importance of this factor: (i) IGF-I also can induce a growth response in Leishmania (Leishmania) mexicana amastigotes; (ii) IGF-I binds specifically to a putative single-site receptor on both promastigotes and amastigotes; (iii) IGF-I induces a rapid tyrosine phosphorylation of parasite proteins with different molecular mass in promastigotes and amastigotes of L. (L.) mexicana; and, finally, (iv) the cutaneous lesion in the mice when challenged by IGF-I-preactivated Leishmania (Viannia) panamensis is increased significantly because of inf lammatory process and growth of parasites. We thus suggest that IGF-I is another important host factor participating in the Leishmania-host interplay in the early stage during the establishment of the infection and presumably also in the later stages.

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Leishmania (Viannia) panamensis - induced cutaneous leishmaniasis in susceptible and resistant mouse strains

Cited by 11 publications

References 16 publications

Endemically exposed asymptomatic individuals show no increase in the specific Leishmania (Viannia) panamensis‐Th1 immune response in comparison to patients with localized cutaneous leishmaniasis

Endemically exposed asymptomatic individuals show no increase in the specific Leishmania (Viannia) panamensis‐Th1 immune response in comparison to patients with localized cutaneous leishmaniasis

Leishmania RNA virus: when the host pays the toll

Insulin-like growth factor I is a growth-promoting factor forLeishmaniapromastigotes and amastigotes

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