THAISE YUMIE TOMOKANE
Projetos de Pesquisa
Unidades Organizacionais
Departamento de Patologia, Faculdade de Medicina
LIM/50 - Laboratório de Patologia das Moléstias Infecciosas, Hospital das Clínicas, Faculdade de Medicina
LIM/50 - Laboratório de Patologia das Moléstias Infecciosas, Hospital das Clínicas, Faculdade de Medicina
4 resultados
Resultados de Busca
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- Macrophage Polarization in the Skin Lesion Caused by Neotropical Species of Leishmania sp(2021) PACHECO, Carmen M. Sandoval; V, Gabriela Araujo Flores; GONZALEZ, Kadir; GOMES, Claudia M. de Castro; PASSERO, Luiz F. D.; TOMOKANE, Thaise Y.; SOSA-OCHOA, Wilfredo; ZUNIGA, Concepcion; CALZADA, Jose; SALDANA, Azael; CORBETT, Carlos E. P.; SILVEIRA, Fernando T.; LAURENTI, Marcia D.Macrophages play important roles in the innate and acquired immune responses against Leishmania parasites. Depending on the subset and activation status, macrophages may eliminate intracellular parasites; however, these host cells also can offer a safe environment for Leishmania replication. In this sense, the fate of the parasite may be influenced by the phenotype of the infected macrophage, linked to the subtype of classically activated (M1) or alternatively activated (M2) macrophages. In the present study, M1 and M2 macrophage subsets were analyzed by double-staining immunohistochemistry in skin biopsies from patients with American cutaneous leishmaniasis (ACL) caused by L. (L.) amazonensis, L. (V.) braziliensis, L. (V.) panamensis ,and L. (L.) infantum chagasi. High number of M1 macrophages was detected in nonulcerated cutaneous leishmaniasis (NUCL) caused by L. (L.) infantum chagasi (M1=112 +/- 12, M2=43 +/- 12 cells/mm(2)). On the other side, high density of M2 macrophages was observed in the skin lesions of patients with anergic diffuse cutaneous leishmaniasis (ADCL) (M1=195 +/- 25, M2=616 +/- 114), followed by cases of localized cutaneous leishmaniasis (LCL) caused by L. (L.) amazonensis (M1=97 +/- 24, M2=219 +/- 29), L. (V.) panamensis (M1=71 +/- 14, M2=164 +/- 14), and L. (V.) braziliensis (M1=50 +/- 13, M2=53 +/- 10); however, low density of M2 macrophages was observed in NUCL. The data presented herein show the polarization of macrophages in skin lesions caused by different Leishmania species that may be related with the outcome of the disease.
- Evaluation of Regulatory Immune Response in Skin Lesions of Patients Affected by Nonulcerated or Atypical Cutaneous Leishmaniasis in Honduras, Central America(2018) FLORES, Gabriela Venicia Araujo; PACHECO, Carmen Maria Sandoval; TOMOKANE, Thaise Yumie; OCHOA, Wilfredo Sosa; VALERIANO, Concepcion Zuniga; GOMES, Claudia Maria Castro; CORBETT, Carlos Eduardo Pereira; LAURENTI, Marcia DalastraIn Honduras, Leishmania (L.) infantum chagasi causes both visceral leishmaniasis (LV) and nonulcerated or atypical cutaneous leishmaniasis (NUCL). NUCL is characterized by mononuclear inflammatory infiltration of the dermis, composed mainly of lymphocytes followed by macrophages with discrete parasitism. Considering that little is known about the pathogenesis of NUCL, the aim of this study was to evaluate the regulatory response in situ in skin lesions of patients affected by NUCL. Biopsies (n = 20) from human cutaneous nonulcerative lesions were collected and processed by usual histological techniques. The in situ regulatory immune response was evaluated by immunohistochemistry using antihuman CD4, FoxP3, IL-10, and TGF-beta antibodies. CD4(+), FoxP3(+), TGF-beta(+), and IL-10(+) cells were observed in the dermis with inflammatory infiltration in all studied cases and at higher densities compared to the normal skin controls. A positive and strong correlation was observed between CD4(+) and FoxP3(+) cells, and a positive and moderate correlation was observed between FoxP3(+) and TGF-beta(+) but not with IL-10(+) cells. The data suggest that T regulatory FoxP3(+) cells and the regulatory cytokines, especially TGF-beta, play an important role in the immunopathogenesis of NUCL, modulating a cellular immune response in the skin, avoiding tissue damage, and leading to low tissue parasitic persistence.
- Evaluation of systemic immunity in atypical cutaneous leishmaniasis caused by Leishmania (L.) infantum chagasi(2022) LAURENTI, Marcia Dalastra; SOSA-OCHOA, Wilfredo; FLORES, Gabriela Venicia Araujo; PACHECO, Carmen Maria Sandoval; TOMOKANE, Thaise Yumie; OLIVEIRA, Luanda Mara da Silva; ZUNIGA, Concepcion; SILVEIRA, Fernando Tobias; CORBETT, Carlos Eduardo PereiraIn some central-American countries, Leishmania (L.) infantum chagasi infection can cause non-ulcerated or atypical cutaneous leishmaniasis (NUCL) in addition to the classic clinical form, visceral leishmaniasis (VL). Little is known about the host-parasite relationship that can contribute to the determination of one or another clinical form. The present study had the objective to evaluate the humoral and cellular immunity in the sera of individuals affected by NUCL to improve the comprehension of this atypical host-parasite interaction. Based on clinical and laboratory diagnosis, serum of 80 individuals was collected to evaluate the cytokines and immunoglobulins profile of NUCL (n = 47), VL patients (n = 5), and negative controls (n = 28). Cytokines were detected using Cytokine Bead Array (CBA) Human Th1/Th2/Th17 kit according to the manufacturer's instructions; class (IgG and IgM), and subclass of (IgG1 and IgG2) immunoglobulins was evaluated by ELISA using specific antigens. The concentration of TNF-alpha, IFN-gamma, IL-2 and IL-4 cytokines in NUCL, VL and control was present below the detection threshold of CBA kit. IL-6, IL-10 and IL-17A cytokines was lower in NUCL compared to LV patients. Regarding to immunoglobulins, NUCL patients produced 4.0 times more IgG than the control, while VL patients produced 6.6 times more; and IgM level was 1.6 times higher in NUCL and 2.6 times in VL patients compared to the control. Concerning the immunoglobulins subclass, only VL patients showed positive reaction for IgG1, and IgG2 did not show positive reaction among the groups. The results showed a weak cellular and humoral systemic immune response in NUCL patients.
- Leishmania (L.) infantum chagasi isolated from skin lesions of patients affected by non-ulcerated cutaneous leishmaniasis lead to visceral lesion in hamsters(2023) FLORES, Gabriela V. Araujo; PACHECO, Carmen M. Sandoval; FERREIRA, Aurea F.; TOMOKANE, Thaise Yumie; NUNES, Juliana B.; COLOMBO, Fabio A.; SOSA-OCHOA, Wilfredo H.; ZUNIGA, Concepcion; SILVEIRA, Fernando T.; CORBETT, Carlos E. P.; LAURENTI, Marcia D.In Central America, Leishmania (L.) infantum chagasi infection causes visceral leishmaniasis (VL) and non -ulcerated cutaneous leishmaniasis (NUCL). The aim of the present study was to evaluate the course of an experimental infection in hamsters caused by L. (L.) infantum chagasi isolated from patients affected by NUCL compared with a strain isolated from a patient with VL. Stationary phase parasites in culture were inoculated through subcutaneous and intraperitoneal routes in hamsters. Following the post-infection times, a histopath-ological study, parasite load and cytokine determination in skin from the cutaneous inoculation site and viscera were performed. Animals subcutaneously infected with the different strains did not develop macroscopic lesions at the inoculation site, and the histopathological changes in the dermis were very slight. Regarding the histo-pathological study of the viscera, we observed the portal mononuclear inflammatory infiltrate, the presence of nodules in the hepatic parenchyma and the proliferation of macrophages in the spleen, which increased over the infection course. Overall, the parasite load in the liver and spleen and in the total IgG titres in the sera of infected hamster showed an increase with the time of infection, regardless of the route of inoculation. Regarding cellular immunity, we did not observe an increase or decrease in pro-and anti-inflammatory cytokines compared to the healthy control, except for IL-10, which was evident in the infected animals. The data showed that strains iso-lated from NUCL cause visceral lesions in the hamsters regardless of the route of inoculation, and they were similar to parasites isolated from VL humans.