Th1/Th2 Cytokine Profile in Patients Coinfected with HIV and Leishmania in Brazil

Rodrigues, Maria Zilma Andrade; Grassi, Maria Fernanda Rios; Mehta, Sanjay R.; Zhang, Xingquan; Gois, Luana Leandro; Schooley, Robert T.; Badaró, Roberto

doi:10.1128/cvi.00076-11

Cited by 12 publications

(6 citation statements)

References 28 publications

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“…In HIV-VL co-infection, the Th2 response that is characteristic of VL is exaggerated, with decreased levels of IL-12 and IL-18 and IFN-γ [30] . In HIV and CL co-infected patients, a similar change was not found in a study with a limited number of patients who had normal IFN-γ levels, but this change may underlie more severe cutaneous disease [31] . Patients co-infected with HIV and tegumentary leishmaniasis (the term used in South America to denote CL, MCL, or DCL) were shown to have decreased absolute numbers of effector and central memory CD4 cells with decreased function as demonstrated by response to stimulation with Leishmania antigen [32] ; however, this defect is not as profound as in HIV-VL co-infections (>350 and <200 CD4 cells/mm 3 , for tegumentary and visceral leishmaniasis, respectively) [33] .…”

Section: Immune Responses In Hiv and Leishmaniasis Co-infectionsupporting

confidence: 57%

PKDL and Other Dermal Lesions in HIV Co-infected Patients with Leishmaniasis: Review of Clinical Presentation in Relation to Immune Responses

Zijlstra¹

2014

PLoS Negl Trop Dis

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BackgroundCo-infection of leishmaniasis and HIV is increasingly reported. The clinical presentation of leishmaniasis is determined by the host immune response to the parasite; as a consequence, this presentation will be influenced by HIV-induced immunosuppression. As leishmaniasis commonly affects the skin, increasing immunosuppression changes the clinical presentation, such as in post-kala-azar dermal leishmaniasis (PKDL) and cutaneous leishmaniasis (CL); dermal lesions are also commonly reported in visceral leishmaniasis (VL) and HIV co-infection.MethodsWe reviewed the literature with regard to dermal manifestations in leishmaniasis and HIV co-infection, in three clinical syndromes, according to the primary presentation: PKDL, VL, or CL.ResultsA wide variety of descriptions of dermal leishmaniasis in HIV co-infection has been reported. Lesions are commonly described as florid, symmetrical, non-ulcerating, nodular lesions with atypical distribution and numerous parasites. Pre-existing, unrelated dermal lesions may become parasitized. Parasites lose their tropism and no longer exclusively cause VL or CL. PKDL in HIV co-infected patients is more common and more severe and is not restricted to Leishmania donovani. In VL, dermal lesions occur in up to 18% of patients and may present as (severe) localized cutaneous leishmaniasis, disseminated cutaneous leishmaniasis (DL) or diffuse cutaneous leishmaniasis (DCL); there may be an overlap with para-kala-azar dermal leishmaniasis. In CL, dissemination in the skin may occur resembling DL or DCL; subsequent spread to the viscera may follow. Mucosal lesions are commonly found in VL or CL and HIV co-infection. Classical mucocutaneous leishmaniasis is more severe. Immune reconstitution disease (IRD) is uncommon in HIV co-infected patients with leishmaniasis on antiretroviral treatment (ART).ConclusionWith increasing immunosuppression, the clinical syndromes of CL, VL, and PKDL become more severe and may overlap. These syndromes may be best described as VL with disseminated cutaneous lesions (before, during, or after VL) and disseminated cutaneous leishmaniasis with or without visceralization.

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Section: Immune Responses In Hiv and Leishmaniasis Co-infectionsupporting

confidence: 57%

PKDL and Other Dermal Lesions in HIV Co-infected Patients with Leishmaniasis: Review of Clinical Presentation in Relation to Immune Responses

Zijlstra¹

2014

PLoS Negl Trop Dis

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“…HIV/ Leishmania co-infected patients also present a reduction in the lymphoproliferative response to Leishmania antigens associated with the decreased quantity of both effector memory and central memory CD4 + T-cells ( Góis et al, 2014 ). A reduction in the IFN-γ and IL-13 levels and the ratio of IFN-γ/IL-10 produced in response to stimulation with soluble Leishmania antigens were also observed in individuals infected with HIV and/or cutaneous leishmaniasis ( Rodrigues et al, 2011 ). They suggested that alterations in cytokines expression create a microenvironment that favors the replication and the spread of the Leishmania parasites, leading to the dissemination of cutaneous infection and the visceralization of typically dermotropic species ( Rodrigues et al, 2011 ).…”

Section: The Host Point Of Viewmentioning

confidence: 98%

The Binomial Parasite-Host Immunity in the Healing Process and in Reactivation of Human Tegumentary Leishmaniasis

2018

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Leishmaniasis is a vector-borne infectious disease caused by different species of protozoa from the Leishmania genus. Classically, the disease can be classified into two main clinical forms: Visceral (VL) and Tegumentary (TL) leishmaniasis. TL is a skin/mucosal granulomatous disease that manifests mainly as cutaneous localized or disseminated ulcers, papules diffusely distributed, mucosal lesions or atypical lesions. Once the etiology of the infection is confirmed, treatment can take place, and different drugs can be administered. It has already been shown that, even when the scar is clinically evident, inflammation is still present in the native tissue, and the decrease of the inflammatory process occurs slowly during the 1st years after clinical healing. The maintenance of residual parasites in the scar tissue is also well documented. Therefore, it is no longer a surprise that, under some circumstances, therapeutic failure and/or lesion reactivation occurs. All over the years, an impressive amount of data on relapses, treatment resistance and lesion reactivation after healing has been collected, and several factors have been pointed out as having a role in the process. Different factors such as Leishmania species, parasite variability, Leishmania RNA virus 1, parasite load, parasite persistence, age, nutritional status, gender, co-morbidities, co-infection, pregnancy, immunosuppression, lesion duration, number and localization of lesions, drug metabolism, irregular treatment and individual host cellular immune response were described and discussed in the present review. Unfortunately, despite this amount of information, a conclusive understanding remains under construction. In addition, multifactorial influence cannot be discarded. In this context, knowing why leishmaniasis has been difficult to treat and control can help the development of new approaches, such as drugs and immunotherapy in order to improve healing maintenance. In this sense, we would like to highlight some of the findings that may influence the course of Leishmania infection and the therapeutic response, with an emphasis on TL.

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“…Additionally, elevated pro-inflammatory cytokine production is considered to be a predictor of IRIS development in HIV-infected patients at the onset of HAART [ 26 ]. Considering the plasma levels of TNF-α in two HIV-uninfected patients with active mucocutaneous leishmaniasis evaluated at our laboratory (22 pg/mL and 13 pg/mL) [ 27 ], the levels observed in this patient during IRIS were similar. Following treatment with Amphotericin B and corticosteroids, an increase in plasmatic IFN-γ, as well as in the IFN-γ/IL-10 ratio, was observed in the present case, while TNF-α remained stable.…”

Section: Discussionmentioning

confidence: 96%

Immune response to Leishmania antigens in an AIDS patient with mucocutaneous leishmaniasis as a manifestation of immune reconstitution inflammatory syndrome (IRIS): a case report

et al. 2015

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BackgroundAfter the onset of HAART, some HIV-infected individuals under treatment present a exacerbated inflammation in response to a latent or a previously treated opportunistic pathogen termed immune reconstitution inflammatory syndrome (IRIS). Few reports of tegumentary leishmaniasis have been described in association with IRIS. Moreover, the immunopathogenesis of IRIS in association with Leishmania is unclear.Case presentationThe present study reports on a 29-year-old HIV-infected individual who developed mucocutaneous leishmaniasis associated with immune reconstitution inflammatory syndrome (IRIS) five months following highly active antiretroviral therapy (HAART). Severe lesions resulted in the partial destruction of the nasal septum, with improvement observed 15 days after treatment with Amphotericin B and corticosteroids. The immune response of this patient was evaluated before and after the lesions healed. IRIS was diagnosed in association with high levels of TNF-α and IL-6. Decreased production of IFN-γ and a low IFN-γ/IL-10 ratio were also observed in response to Leishmania antigens. After receiving anti-leishmanial treatment, the individual’s specific Th1 immune response was restored.ConclusionThe results suggest that the production of inflammatory cytokines by unstimulated T-lymphocytes could contribute to occurrence of leishmaniasis associated with IRIS.

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Th1/Th2 Cytokine Profile in Patients Coinfected with HIV and Leishmania in Brazil

Cited by 12 publications

References 28 publications

PKDL and Other Dermal Lesions in HIV Co-infected Patients with Leishmaniasis: Review of Clinical Presentation in Relation to Immune Responses

PKDL and Other Dermal Lesions in HIV Co-infected Patients with Leishmaniasis: Review of Clinical Presentation in Relation to Immune Responses

The Binomial Parasite-Host Immunity in the Healing Process and in Reactivation of Human Tegumentary Leishmaniasis

Immune response to Leishmania antigens in an AIDS patient with mucocutaneous leishmaniasis as a manifestation of immune reconstitution inflammatory syndrome (IRIS): a case report

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