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Search Results: 1 - 10 of 452346 matches for " Da-Cruz Alda M "
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Atypical Mucocutaneous Leishmaniasis Caused by Leishmania braziliensis in an Acquired Immunodeficiency Syndrome Patient: T-cell Responses and Remission of Lesions Associated with Antigen Immunotherapy
Da-Cruz Alda M,Filgueiras Danilo V,Coutinho Ziadir,Mayrink Wilson
Memórias do Instituto Oswaldo Cruz , 1999,
Abstract: An atypical case of acquired immunodeficiency syndrome-associated mucocutaneous lesions due to Leishmania braziliensis is described. Many vacuolated macrophages laden with amastigote forms of the parasite were found in the lesions. Leishmanin skin test and serology for leishmaniasis were both negative. The patient was resistant to therapy with conventional drugs (antimonial and amphotericin B). Interestingly, remission of lesions was achieved after an alternative combined therapy of antimonial associated with immunotherapy (whole promastigote antigens). Peripheral blood mononuclear cells were separated and stimulated in vitro with Leishmania antigens to test the lymphoproliferative responses (LPR). Before the combined immunochemotherapy, the LPR to leishmanial antigens was negligible (stimulation index - SI=1.4). After the first course of combined therapy it became positive (SI=4.17). The antigen responding cells were predominantly T-cells (47.5%) most of them with CD8+ phenotype (33%). Very low CD4+ cells (2.2%) percentages were detected. The increased T-cell responsiveness to leishmanial antigens after combined therapy was accompanied by interferon-g (IFN-g) production as observed in the cell culture supernatants. In this patient, healing of the leishmaniasis lesions was associated with the induction of a specific T-cell immune response, characterized by the production of IFN-g and the predominance of the CD8+ phenotype among the Leishmania-reactive T-cells.
Atypical Mucocutaneous Leishmaniasis Caused by Leishmania braziliensis in an Acquired Immunodeficiency Syndrome Patient: T-cell Responses and Remission of Lesions Associated with Antigen Immunotherapy
Da-Cruz, Alda M;Filgueiras, Danilo V;Coutinho, Ziadir;Mayrink, Wilson;Grimaldi Jr, Gabriel;De Luca, Paula M;Mendon?a, Sergio CF;Coutinho, Sergio G;
Memórias do Instituto Oswaldo Cruz , 1999, DOI: 10.1590/S0074-02761999000400020
Abstract: an atypical case of acquired immunodeficiency syndrome-associated mucocutaneous lesions due to leishmania braziliensis is described. many vacuolated macrophages laden with amastigote forms of the parasite were found in the lesions. leishmanin skin test and serology for leishmaniasis were both negative. the patient was resistant to therapy with conventional drugs (antimonial and amphotericin b). interestingly, remission of lesions was achieved after an alternative combined therapy of antimonial associated with immunotherapy (whole promastigote antigens). peripheral blood mononuclear cells were separated and stimulated in vitro with leishmania antigens to test the lymphoproliferative responses (lpr). before the combined immunochemotherapy, the lpr to leishmanial antigens was negligible (stimulation index - si=1.4). after the first course of combined therapy it became positive (si=4.17). the antigen responding cells were predominantly t-cells (47.5%) most of them with cd8+ phenotype (33%). very low cd4+ cells (2.2%) percentages were detected. the increased t-cell responsiveness to leishmanial antigens after combined therapy was accompanied by interferon-g (ifn-g) production as observed in the cell culture supernatants. in this patient, healing of the leishmaniasis lesions was associated with the induction of a specific t-cell immune response, characterized by the production of ifn-g and the predominance of the cd8+ phenotype among the leishmania-reactive t-cells.
Evidence That Lipopolisaccharide May Contribute to the Cytokine Storm and Cellular Activation in Patients with Visceral Leishmaniasis
Joanna R. Santos-Oliveira,Eduardo G. Regis,Cássia R. B. Leal,Rivaldo V. Cunha,Patrícia T. Bozza,Alda M. Da-Cruz
PLOS Neglected Tropical Diseases , 2011, DOI: 10.1371/journal.pntd.0001198
Abstract: Background Visceral leishmaniasis (VL) is characterized by parasite-specific immunosuppression besides an intense pro-inflammatory response. Lipopolisaccharide (LPS) has been implicated in the immune activation of T-cell deficient diseases such as HIV/AIDS and idiopathic lymphocytopenia. The source of LPS is gram-negative bacteria that enter the circulation because of immunological mucosal barrier breakdown. As gut parasitization also occurs in VL, it was hypothesized that LPS may be elevated in leishmaniasis, contributing to cell activation. Methodology/Principal Findings Flow cytometry analysis and immunoassays (ELISA and luminex micro-beads system) were used to quantify T-cells and soluble factors. Higher LPS and soluble CD14 levels were observed in active VL in comparison to healthy subjects, indicating that LPS was bioactive; there was a positive correlation between these molecules (r = 0.61;p<0.05). Interestingly, LPS was negatively correlated with CD4+ (r = ?0.71;p<0.01) and CD8+ T-cells (r = ?0.65;p<0.05). Moreover, higher levels of activation-associated molecules (HLA-DR, CD38, CD25) were seen on T lymphocytes, which were positively associated with LPS levels. Pro-inflammatory cytokines and macrophage migration inhibitory factor (MIF) were also augmented in VL patients. Consistent with the higher immune activation status, LPS levels were positively correlated with the inflammatory cytokines IL-6 (r = 0.63;p<0.05), IL-8 (r = 0.89;p<0.05), and MIF (r = 0.64;p<0.05). Also, higher plasma intestinal fatty acid binding protein (IFABP) levels were observed in VL patients, which correlated with LPS levels (r = 0.57;p<0.05). Conclusions/Significance Elevated levels of LPS in VL, in correlation with T-cell activation and elevated pro-inflammatory cytokines and MIF indicate that this bacterial product may contribute to the impairment in immune effector function. The cytokine storm and chronic immune hyperactivation status may contribute to the observed T-cell depletion. LPS probably originates from microbial translocation as suggested by IFABP levels and, along with Leishmania antigen-mediated immune suppression, may play a role in the immunopathogenesis of VL. These findings point to possible benefits of antimicrobial prophylaxis in conjunction with anti-Leishmania therapy.
Chagas' Disease and HIV Co-infection: Genotypic Characterization of the Trypanosoma cruzi Strain
Pacheco, Raquel S;Ferreira, Marcelo S;Machado, Maria Inês;Brito, Célia MM;Pires, Marize Q;Da-Cruz, Alda M;Coutinho, Sérgio G;
Memórias do Instituto Oswaldo Cruz , 1998, DOI: 10.1590/S0074-02761998000200005
Abstract: in the past few years, new aspects of the immunopathology of chagas' disease have been described in immunosuppressed patients, such as fatal central nervous system lesions related to the reactivation of the parasite. this article is the first description of the genotypic characterization, at the strain level, of trypanosoma cruzi isolated from a patient with chagas` disease/aids co-infection. the presence of four hypodense lesions was observed in the cranial compute tomographic scan. the diagnosis of aids was assessed by the detection of anti-hiv antibodies using enzyme-linked immunosorbent assay (elisa) and western blot techniques. the cd4+ lymphocyte counts were maintained under 200 cells/mm3 during one year demonstrating the severity of the state of immunosuppression. chagas' disease was confirmed by serological and parasitological methods. trypomastigote forms were visualized in a thick blood smear. the parasite isolated is genotypically similar to the cl strain. the paper reinforces that cerebral chagas' disease can be considered as another potential opportunistic infection in aids resulting from the reactivation of a dormant t. cruzi infection acquired years earlier.
Tumor necrosis factor-α in human American tegumentary leishmaniasis
Da-Cruz, Alda Maria;Oliveira, Márcia Pereira de;De Luca, Paula Mello;Mendon?a, Sergio CF;Coutinho, Sergio G;
Memórias do Instituto Oswaldo Cruz , 1996, DOI: 10.1590/S0074-02761996000200019
Abstract: tumor necrosis factor-alpha (tnf-α) is a cytokine produced by activated macrophages and other cells. in order to verify whether the serum levels of tnf-α in american tegumentary leishmaniasis patients are associated with the process of cure or aggravation of the disease, 41 patients were studied: 26 cases of cutaneous leishmaniasis (cl) and 15 of mucocutaneous leishmaniasis (mcl). during active disease the serum levels of tnf-α of mcl patients were significantly higher than those of cl patients and control subjects (healthy individuals and cutaneous lesions from other etiologies). the mcl patients had serum titers of tnf-α significantly lower at the end of antimonial therapy than before therapy. after a six-month follow-up, the mcl patients had serum levels of tnf-α similar to those observed at the end of the therapy as well as to those of cl patients and control subjects. no significant variation in the serum levels of tnf-α was observed in cl patients throughout the study period (before, at the end of therapy and after a six-month follow-up). the possible relationship between the high tnf-α serum levels and severity of the disease is discussed.
Disseminated American muco-cutaneous leishmaniasis caused by Leishmania brasiliensis brasiliensis in a patient with AIDS: a case report
Machado, Elizabeth S.;Braga, Maria da Providencia;Da-Cruz, Alda Maria;Coutinho, Sérgio G.;Vieira, Alba Regina M.;Rutowitsch, Marcio S.;Cuzzi-Maya, Tulia;Grimaldi Junior, Gabriel;Menezes, Jacquelie A.;
Memórias do Instituto Oswaldo Cruz , 1992, DOI: 10.1590/S0074-02761992000400005
Abstract: the authors report a case of culture-proven disseminated american muco-cutaneous leishmaniasis caused by leishmania brasiliensis brasiliensis in an hiv positive patient. lesions began in the oropharynx and nasal mucosa eventually spreading to much of the skin surface. the response to a short course of glucantime therapy was good.
High levels of T lymphocyte activation in Leishmania-HIV-1 co-infected individuals despite low HIV viral load
Joanna R Santos-Oliveira, Carmem BW Giacoia-Gripp, Priscilla Alexandrino de Oliveira, Valdir S Amato, Jose Lindoso, Hiro Goto, Manoel P Oliveira-Neto, Marise S Mattos, Beatriz Grinsztejn, Mariza G Morgado, Alda M Da-Cruz
BMC Infectious Diseases , 2010, DOI: 10.1186/1471-2334-10-358
Abstract: To address this issue we analyzed CD4+ T absolute counts and the proportion of CD8+ T cells expressing CD38 in Leishmania/HIV co-infected patients that recovered after anti-leishmanial therapy.We found that, despite clinical remission of leishmaniasis, AVL co-infected patients presented a more severe immunossupression as suggested by CD4+ T cell counts under 200 cells/mm3, differing from ATL/HIV-AIDS cases that tends to show higher lymphocytes levels (over 350 cells/mm3). Furthermore, five out of nine, AVL/HIV-AIDS presented low CD4+ T cell counts in spite of low or undetectable viral load. Expression of CD38 on CD8+ T lymphocytes was significantly higher in AVL or ATL/HIV-AIDS cases compared to HIV/AIDS patients without leishmaniasis or healthy subjects.Leishmania infection can increase the degree of immune system activation in individuals concomitantly infected with HIV. In addition, AVL/HIV-AIDS patients can present low CD4+ T cell counts and higher proportion of activated T lymphocytes even when HIV viral load is suppressed under HAART. This fact can cause a misinterpretation of these laboratorial markers in co-infected patients.Leishmania/HIV-1 co-infection has been considered an emerging disease mainly due to the expansion of the AIDS epidemic over leishmaniasis endemic areas and vice-versa [1]. Visceral leishmaniasis associated-HIV/AIDS is well known as an opportunistic disease especially in the Mediterranean basin [1]. However, an increasing number of reports of tegumentary leishmaniasis-HIV/AIDS patients underlines the importance of this additional association [2-6]. In America, vector sandflies and Leishmania species that cause American visceral leishmaniasis (AVL) and tegumentary leishmaniasis (ATL) differ from those observed in other endemic regions around the world. This could result in the particular clinical features observed in HIV-co-infected patients in the New World [3,7]. In Brazil, both Leishmania and HIV infection are endemic and this co-infect
T-cell responses associated with resistance to Leishmania infection in individuals from endemic areas for Leishmania (Viannia) braziliensis
Bittar, Rita C;Nogueira, Ricardo S;Vieira-Gon?alves, Ricardo;Pinho-Ribeiro, Vanessa;Mattos, Marise S;Oliveira-Neto, Manoel Paes;Coutinho, Sergio G;Da-Cruz, Alda M;
Memórias do Instituto Oswaldo Cruz , 2007, DOI: 10.1590/S0074-02762007005000069
Abstract: subclinical or asymptomatic infection is documented in individuals living in endemic areas for leishmaniasis suggesting that the development of an appropriate immune response can control parasite replication and maintain tissue integrity. a low morbidity indicates that intrinsic factors could favor resistance to leishmania infection. herein, leishmanial t-cell responses induced in subjects with low susceptibility to leishmaniasis as asymptomatic subjects were compared to those observed in cured cutaneous leishmaniasis (ccl) patients, who controlled the disease after antimonial therapy. all of them have shown maintenance of specific long-term immune responses characterized by expansion of higher proportions of cd4+ as compared to cd8+ leishmania reactive t-lymphocytes. asymptomatic subjects had lower indexes of in vitro leishmania induced lymphoproliferative responses and interferon-gamma (ifn-g) production in comparison to ccl patients. on the other hand, interleukin (il-10) production was much higher in asymptomatics than in ccl, while no differences in il-5 levels were found. in conclusion, long lived t-cell responses achieved by asymptomatic individuals differed from those who had developed symptomatic leishmaniasis in terms of intensity of lymphocyte activation (proliferation or ifn-g) and regulatory mechanisms (il-10). the absence of the disease in asymptomatics could be explained by their intrinsic ability to create a balance between immunoregulatory (il-10) and effector cytokines (ifn-g), leading to parasite destruction without producing skin tissue damage. the establishment of profiles of cell-mediated immune responses associated with resistance against leishmania infection is likely to make new inroads into understanding the long-lived immune protection against the disease.
Leishmania?braziliensis-Reactive T Cells Are Down-Regulated in Long-Term Cured Cutaneous Leishmaniasis, but the Renewal Capacity of T Effector Memory Compartments Is Preserved
Regina Pereira-Carvalho, Carolina O. Mendes-Aguiar, Manoel P. Oliveira-Neto, Cláudia J. F. Covas, álvaro L. Bertho, Alda M. Da-Cruz, Adriano Gomes-Silva
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0081529
Abstract: Leishmania?(Viannia)?braziliensis control and tissue damage relate to the effector immune response, which in turn affects clinical outcome. Leishmania reactive CD4+ and CD8+ T cells are expanded in long-term healed cutaneous leishmaniasis (hCL) patients but their functional characteristics remain to be determined. This study investigates antigen-specific recall in long-term healed CL caused by L.?braziliensis infection. Healed CL subjects were grouped according to the time elapsed since the end of therapy: less than two years and two to five years. Activation phenotype (CD69+ or CD25+) and subpopulations of memory T cell phenotypes [central memory (Tcm): CD45RO+ CCR7+ or effector memory (Tem): CD45RO+ CCR7-] were quantified in ex vivo blood mononuclear cells and after Leishmania antigens stimuli. A reduction in the percentage of activated Leishmania-responder CD4+ and CD8+ T cells in hCL was associated with the time elapsed since clinical cure. Percentage of CD69+ in TCD4+ and TCD8+ cells were negatively correlated with IL-10 levels. Ex vivo analyses showed contracted Tem CD4+ and Tem CD8+ compartments from hCL with long time elapsed since clinical cure, although renewal of these compartments was observed following in vitro exposure to leishmanial stimuli. Our results show that healed L.?braziliensis infected patients exhibit a recall response to Leishmania antigens with evident expansion of effector memory T cells. Regulated leishmanial-specific response seems to emerge only about two years after initial contact with the parasite antigens.
Lipopolysaccharide-Induced Cellular Activation May Participate in the Immunopathogenesis of Visceral Leishmaniasis Alone or in HIV Coinfection
Joanna Reis Santos-Oliveira,Alda Maria Da-Cruz
International Journal of Microbiology , 2012, DOI: 10.1155/2012/364534
Abstract: Visceral Leishmaniasis (VL) is an infectious disease which constitutes a serious public health problem, integrating the list of neglected tropical diseases. The disease is characterized by a Leishmania-specific immune suppression T-cell depletion and a decrease of other hematopoietic cells. In parallel, an immunostimulatory response also occurs, represented by polyclonal B lymphocytes, T-cell activation, and systemic proinflammatory responses. Parasite antigens were believed to mediate both suppression and activation mechanisms, but these concepts are constantly being revised. Similar to reports on HIV/AIDS, we have proposed that gut parasitation by amastigotes and lymphocyte depletion could also affect gut-associated lymphoid tissue, leading to mucosal barrier breach and predisposing to microbial translocation. An increment of plasmatic lipopolysaccharide (LPS) levels observed in Brazilian VL patients was implicated in the reduced blood CD4
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