CD4+ and CD8+ T Cell Immune Responses of Immunocompetent and Immunocompromised (AIDS) Patients with American Tegumentary Leishmaniasis

Submitted by Sandra Infurna ([email protected]) on 2019-11-07T17:12:28Z No. of bitstreams: 1 AldaMCruz_Paula_Lucca_etal_IOC_1996.pdf: 67487 bytes, checksum: d21a1f4ad327f8eccea6d44b26edab3b (MD5)Approved for entry into archive by Sandra Infurna ([email protected]) on 2019-11-07T17:18:07Z (GMT) No. of bitstreams: 1 AldaMCruz_Paula_Lucca_etal_IOC_1996.pdf: 67487 bytes, checksum: d21a1f4ad327f8eccea6d44b26edab3b (MD5)Made available in DSpace on 2019-11-07T17:18:07Z (GMT). No. of bitstreams: 1 AldaMCruz_Paula_Lucca_etal_IOC_1996.pdf: 67487 bytes, checksum: d21a1f4ad327f8eccea6d44b26edab3b (MD5) Previous issue date: 1996Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Departamento de Protozoologia. Laboratório Imunidade Celular e Humoral. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Departamento de Protozoologia. Laboratório Imunidade Celular e Humoral. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Departamento de Protozoologia. Laboratório Imunidade Celular e Humoral. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Departamento de Protozoologia. Laboratório Imunidade Celular e Humoral. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Departamento de Protozoologia. Laboratório Imunidade Celular e Humoral. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Departamento de Protozoologia. Laboratório Imunidade Celular e Humoral. Rio de Janeiro, RJ, Brasil

CD4+ and CD8+ T cell immune responses of immunocompetent and immunocompromised (AIDS) patients with american tegumentary leishmaniasis

Submitted by Sandra Infurna ([email protected]) on 2019-11-07T17:12:28Z No. of bitstreams: 1 AldaMCruz_Paula_Lucca_etal_IOC_1996.pdf: 67487 bytes, checksum: d21a1f4ad327f8eccea6d44b26edab3b (MD5)Approved for entry into archive by Sandra Infurna ([email protected]) on 2019-11-07T17:18:07Z (GMT) No. of bitstreams: 1 AldaMCruz_Paula_Lucca_etal_IOC_1996.pdf: 67487 bytes, checksum: d21a1f4ad327f8eccea6d44b26edab3b (MD5)Made available in DSpace on 2019-11-07T17:18:07Z (GMT). No. of bitstreams: 1 AldaMCruz_Paula_Lucca_etal_IOC_1996.pdf: 67487 bytes, checksum: d21a1f4ad327f8eccea6d44b26edab3b (MD5) Previous issue date: 1996Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Departamento de Protozoologia. Laboratório Imunidade Celular e Humoral. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Departamento de Protozoologia. Laboratório Imunidade Celular e Humoral. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Departamento de Protozoologia. Laboratório Imunidade Celular e Humoral. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Departamento de Protozoologia. Laboratório Imunidade Celular e Humoral. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Departamento de Protozoologia. Laboratório Imunidade Celular e Humoral. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Departamento de Protozoologia. Laboratório Imunidade Celular e Humoral. Rio de Janeiro, RJ, Brasil

High levels of filamentous actin and apoptosis correlate with mast cell refractoriness under alloxan-evoked diabetes

Submitted by Sandra Infurna ([email protected]) on 2019-12-31T18:02:17Z No. of bitstreams: 1 EmilianoBarreto_etal_IOC_2006.pdf: 458212 bytes, checksum: e9aae2b07e337f975cfe1755124fd360 (MD5)Approved for entry into archive by Sandra Infurna ([email protected]) on 2019-12-31T18:13:22Z (GMT) No. of bitstreams: 1 EmilianoBarreto_etal_IOC_2006.pdf: 458212 bytes, checksum: e9aae2b07e337f975cfe1755124fd360 (MD5)Made available in DSpace on 2019-12-31T18:13:22Z (GMT). No. of bitstreams: 1 EmilianoBarreto_etal_IOC_2006.pdf: 458212 bytes, checksum: e9aae2b07e337f975cfe1755124fd360 (MD5) Previous issue date: 2006Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Departamento de Fisiologia e Farmacodinâmica. Laboratório de Inflamação. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Departamento de Fisiologia e Farmacodinâmica. Laboratório de Inflamação. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Departamento de Fisiologia e Farmacodinâmica. Laboratório de Inflamação. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Departamento de Imunologia. Laboratório de Imunoparasitologia. Rio de Janeiro, RJ, Brasil.Universidade do Estado do Rio de Janeiro. Departamento de Farmacologia. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Departamento de Fisiologia e Farmacodinâmica. Laboratório de Inflamação. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Departamento de Fisiologia e Farmacodinâmica. Laboratório de Inflamação. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Departamento de Fisiologia e Farmacodinâmica. Laboratório de Inflamação. Rio de Janeiro, RJ, Brasil.Mast cell number and reactivity were shown to be down-regulated under diabetic conditions. Since the balance between globular and filamentous actin plays a pivotal role in the activity of secretory cells, we investigated whether an imbalance in that system could underlie the hyporesponsiveness of mast cells in diabetes. The apoptotic state was also evaluated. By means of rhodamine/phalloidine staining of F-actin, we noted that diabetic mast cells exhibited an increase in fluorescence intensity and reduction in cellular size, when compared with cells from normal animals, in parallel with elevation in the percentage of cells developing apoptosis. The levels of Bax, a pro-apoptotic member of Bcl-2 family, appeared increased at baseline in mast cells from diabetic rats compared with normal cells. These phenomena correlated with reduction in histamine and PGD2 release following antigen challenge in vitro. The steroid antagonist RU 486 abolished the reduction of histamine secretion from diabetic mast cells. We conclude that hyporesponsiveness of mast cells noted in diabetes may be accounted for by reduction in actin filament plasticity, in clear association with the rise in the percentage of cells undergoing apoptosis. In addition, the refractoriness of diabetic mast cells to antigen in vitro seems to be dependent on glucocorticoids

Carajurin Induces Apoptosis in Leishmania amazonensis Promastigotes through Reactive Oxygen Species Production and Mitochondrial Dysfunction

Carajurin is the main constituent of Arrabidaea chica species with reported anti-Leishmania activity. However, its mechanism of action has not been described. This study investigated the mechanisms of action of carajurin against promastigote forms of Leishmania amazonensis. Carajurin was effective against promastigotes with IC50 of 7.96 ± 1.23 μg.mL−1 (26.4 µM), and the cytotoxic concentration for peritoneal macrophages was 258.2 ± 1.20 μg.mL−1 (856.9 µM) after 24 h of treatment. Ultrastructural evaluation highlighted pronounced swelling of the kinetoplast with loss of electron-density in L. amazonensis promastigotes induced by carajurin treatment. It was observed that carajurin leads to a decrease in the mitochondrial membrane potential (p = 0.0286), an increase in reactive oxygen species production (p = 0.0286), and cell death by late apoptosis (p = 0.0095) in parasites. Pretreatment with the antioxidant NAC prevented ROS production and significantly reduced carajurin-induced cell death. The electrochemical and density functional theory (DFT) data contributed to support the molecular mechanism of action of carajurin associated with the ROS generation, for which it is possible to observe a correlation between the LUMO energy and the electroactivity of carajurin in the presence of molecular oxygen. All these results suggest that carajurin targets the mitochondria in L. amazonensis. In addition, when assessed for its drug-likeness, carajurin follows Lipinski’’s rule of five, and the Ghose, Veber, Egan, and Muegge criteria