Clinical features of cutaneous and disseminated cutaneous leishmaniasis caused by <i>Leishmania (Viannia) braziliensis</i> in Paraty, Rio de Janeiro

Vieira-Gonçalves, Ricardo; Pirmez, Claude; Jorge, Maria Eugenia; Souza, Wilson Jacinto Silva de; Oliveira, Márcia Pereira de; Rutowitsch, M; Da‐Cruz, Alda Maria

doi:10.1111/j.1365-4632.2008.03701.x

Cited by 24 publications

(17 citation statements)

References 29 publications

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“…However, in ATL this polarization is not so clear, being detected Th1 as well as Th2 cytokines in cutaneous or mucosal lesions with a predominance of Th1 cytokines [23,28,44]. In some ATL lesions it is possible to detect tuberculoid granuloma [23,45]. The presence of IL-32 in giant cells in ATL granuloma suggests the involvement of this cytokine in tuberculoid granuloma that deserves further investigation.…”

Section: Discussionmentioning

confidence: 99%

Interleukin 32γ (IL-32γ) is highly expressed in cutaneous and mucosal lesions of American Tegumentary Leishmaniasis patients: association with tumor necrosis factor (TNF) and IL-10

et al. 2014

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BackgroundThe interleukin 32 (IL-32) is a proinflammatory cytokine produced by immune and non-immune cells. It can be induced during bacterial and viral infections, but its production was never investigated in protozoan infections. American Tegumentary Leishmaniasis (ATL) is caused by Leishmania protozoan leading to cutaneous, nasal or oral lesions. The aim of this study was to evaluate the expression of IL-32 in cutaneous and mucosal lesions as well as in peripheral blood mononuclear cells (PBMC) exposed to Leishmania (Viannia) braziliensis.MethodsIL-32, tumour necrosis factor (TNF) and IL-10 protein expression was evaluated by immunohistochemistry in cutaneous, mucosal lesions and compared to healthy specimens. The isoforms of IL-32α, β, δ, γ mRNA, TNF mRNA and IL-10 mRNA were assessed by qPCR in tissue biopsies of lesions and healthy skin and mucosa. In addition, PBMC from healthy donors were cultured with amastigotes of L. (V.) braziliensis. In lesions, the parasite subgenus was identified by PCR-RFLP.ResultsWe showed that the mRNA expression of IL-32, in particular IL-32γ was similarly up-regulated in lesions of cutaneous (CL) or mucosal (ML) leishmaniasis patients. IL-32 protein was produced by epithelial, endothelial, mononuclear cells and giant cells. The IL-32 protein expression was associated with TNF in ML but not in CL. IL-32 was not associated with IL-10 in both CL and ML. Expression of TNF mRNA was higher in ML than in CL lesions, however levels of IL-10 mRNA were similar in both clinical forms. In all lesions in which the parasite was detected, L. (Viannia) subgenus was identified. Interestingly, L. (V.) braziliensis induced only IL-32γ mRNA expression in PBMC from healthy individuals.ConclusionsThese data suggest that IL-32 plays a major role in the inflammatory process caused by L. (Viannia) sp or that IL-32 is crucial for controlling the L. (Viannia) sp infection.

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Section: Discussionmentioning

confidence: 99%

Interleukin 32γ (IL-32γ) is highly expressed in cutaneous and mucosal lesions of American Tegumentary Leishmaniasis patients: association with tumor necrosis factor (TNF) and IL-10

et al. 2014

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“…There are different species of this parasite, which can cause a spectrum of clinical phenotype in humans, ranging from self-healing cutaneous, mucocutaneous skin ulcers to a fatal visceral form. In addition, cutaneous leishmaniases, frequently, are associated to the disfigurement and social stigmatization in patients (Vieira-Gonçalves et al 2008). In Brazil, the species with high medical importance are Leishmania (Viannia) braziliensis and L. (Leishmania) amazonensis.…”

Section: Introductionmentioning

confidence: 99%

Anti-leishmanial effects of purified compounds from aerial parts of Baccharis uncinella C. DC. (Asteraceae)

et al. 2010

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Species of Baccharis exhibit antibiotic, antiseptic, wound-healing, and anti-protozoal properties, and have been used in the traditional medicine of South America for the treatment of several diseases. In the present work, the fractionation of EtOH extract from aerial parts of Baccharis uncinella indicated that the isolated compounds caffeic acid and pectolinaringenin showed inhibitory activity against Leishmania (L.) amazonensis and Leishmania (V.) braziliensis promastigotes, respectively. Moreover, amastigote forms of both species were highly sensible to the fraction composed by oleanolic + ursolic acids and pectolinaringenin. Caffeic acid also inhibited amastigote forms of L. (L.) amazonensis, but this effect was weak in L. (V.) braziliensis amastigotes. The treatment of infected macrophages with these compounds did not alter the levels of nitrates, indicating a direct effect of the compounds on amastigote stages. The results presented herein suggest that the active components from B. uncinella can be important to the design of new drugs against American tegumentar leishmaniases.

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“…Patients had acquired the disease in endemic areas for L. braziliensis infection in Rio de Janeiro, Brazil. The diagnosis of active cutaneous leishmaniasis (A-CL) was confirmed by clinical, parasitological and immunological criteria as described elsewhere [30]. Patients were treated with pentavalent antimonial (N-methyl-glucamine), according to the guidelines of the Brazilian Ministry of Health, and then followed-up.…”

Section: Patientsmentioning

confidence: 99%

The skin homing receptor cutaneous leucocyte-associated antigen (CLA) is up-regulated byLeishmaniaantigens in T lymphocytes during active cutaneous leishmaniasis

Mendes-Aguiar¹,

Gomes-Silva²,

Nunes

et al. 2009

Clinical and Experimental Immunology

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SummaryThe cutaneous leucocyte-associated antigen receptor (CLA) can direct Leishmania-specific T lymphocytes towards inflamed skin lesions. Homing receptors [CLA, lymphocyte-associated antigen 1 (LFA-1) or CD62L] were analysed in lymphocytes from blood and cutaneous leishmaniasis (CL) lesions. CL patients with active lesions (A-CL) presented lower levels of T lymphocytes expressing the CLA + phenotype (T CD4 + = 10·4% Ϯ 7·5% and T CD8 + = 5·8% Ϯ 3·4%) than did healthy subjects (HS) (T CD4 + = 19·3% Ϯ 13·1% and T CD8 + = 21·6% Ϯ 8·8%), notably in T CD8 + (P < 0·001). In clinically cured patients these percentages returned to levels observed in HS. Leishmanial antigens up-regulated CLA in T cells (CLA + in T CD4 + = 33·3% Ϯ 14·1%; CLA + in T CD8 + = 22·4% Ϯ 9·4%) from A-CL but not from HS. An enrichment of CLA + cells was observed in lesions (CLA + in T CD4 + = 45·9% Ϯ 22·5%; CLA + in T CD8 + = 46·4% Ϯ 16·1%) in comparison with blood (CLA + in T CD4 + = 10·4% Ϯ 7·5%; CLA + in T CD8 + = 5·8% Ϯ 3·4%). Conversely, LFA-1 was highly expressed in CD8+ T cells and augmented in CD4+ T from peripheral blood of A-CL patients. In contrast, CD62L was not affected. These results suggest that Leishmania antigens can modulate molecules responsible for migration to skin lesions, potentially influencing the cell composition of inflammatory infiltrate of leishmaniasis or even the severity of the disease.

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Clinical features of cutaneous and disseminated cutaneous leishmaniasis caused by Leishmania (Viannia) braziliensis in Paraty, Rio de Janeiro

Abstract: ATL in Paraty shares the clinical and laboratory characteristics reported for ATL in other regions of RJ, probably because of the similar epidemiologic context related to the Atlantic rainforest region.

Cited by 24 publications

References 29 publications

Interleukin 32γ (IL-32γ) is highly expressed in cutaneous and mucosal lesions of American Tegumentary Leishmaniasis patients: association with tumor necrosis factor (TNF) and IL-10

Interleukin 32γ (IL-32γ) is highly expressed in cutaneous and mucosal lesions of American Tegumentary Leishmaniasis patients: association with tumor necrosis factor (TNF) and IL-10

Anti-leishmanial effects of purified compounds from aerial parts of Baccharis uncinella C. DC. (Asteraceae)

The skin homing receptor cutaneous leucocyte-associated antigen (CLA) is up-regulated byLeishmaniaantigens in T lymphocytes during active cutaneous leishmaniasis

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