Santa Cruz Cabrália, Brazil
Santa Cruz Cabrália, Brazil

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Rodrigues-da-Silva R.N.,Laboratorio Of Imunoparasitologia | Lima-Junior J.C.,Laboratorio Of Imunoparasitologia | Fonseca e Fonseca B.P.,Laboratorio Of Tecnologia Diagnostica | Zuquim Antas P.R.,Laboratorio Of Imunologia Clinica | And 4 more authors.
Memorias do Instituto Oswaldo Cruz | Year: 2014

Haematological and cytokine alterations in malaria are a broad and controversial subject in the literature. However, few studies have simultaneously evaluated various cytokines in a single patient group during the acute and convalescent phases of infection. The aim of this study was to sequentially characterise alterations in haematological patters and circulating plasma cytokine and chemokine levels in patients infected with Plasmodium vivax or Plasmodium falciparum from a Brazilian endemic area during the acute and convalescent phases of infection. During the acute phase, thrombocytopaenia, eosinopaenia, lymphopaenia and an increased number of band cells were observed in the majority of the patients. During the convalescent phase, the haematologic parameters returned to normal. During the acute phase, P. vivax and P. falciparum patients had significantly higher interleukin (IL)-6, IL-8, IL-17, interferon-γ, tumour necrosis factor (TNF)-α, macrophage inflammatory protein-1β and granulocyte-colony stimulating factor levels than controls and maintained high levels during the convalescent phase. IL-10 was detected at high concentrations during the acute phase, but returned to normal levels during the convalescent phase. Plasma IL-10 concentration was positively correlated with parasitaemia in P. vivax and P. falciparum-infected patients. The same was true for the TNF-α concentration in P. falciparum-infected patients. Finally, the haematological and cytokine profiles were similar between uncomplicated P. falciparum and P. vivax infections.


de Pinho R.T.,Laboratorio Of Imunologia Clinica | da Silva W.S.,Laboratorio Of Imunologia Clinica | de Castro COrtes L.M.,Laboratorio Of Biologia Molecular E Doencas Endemicas Ioc Fiocruz | da Silva Vasconcelos Sousa P.,Laboratorio Of Imunologia Clinica | And 3 more authors.
Experimental Parasitology | Year: 2014

Matrix metalloproteinases (MMPs) constitute a large family of Zn2+ and Ca2+ dependent endopeptidases implicated in tissue remodeling and chronic inflammation. MMPs also play key roles in the activation of growth factors, chemokines and cytokines produced by many cell types, including lymphocytes, granulocytes, and, in particular, activated macrophages. Their synthesis and secretion appear to be important in a number of physiological processes, including the inflammatory process. Here, we investigated the interaction between human and mouse macrophages with T.cruzi Colombian and Y strains to characterize MMP-9 and cytokine production in this system. Supernatants and total extract of T.cruzi infected human and mouse macrophages were obtained and used to assess MMP-9 profile and inflammatory cytokines. The presence of metalloproteinase activity was determined by zymography, enzyme-linked immunosorbent assay and immunoblotting assays. The effect of cytokines on MMP-9 production in human macrophages was verified by previous incubation of cytokines on these cells in culture, and analyzed by zymography. We detected an increase in MMP-9 production in the culture supernatants of T.cruzi infected human and mouse macrophages. The addition of IL-1β or TNF-α to human macrophage cultures increased MMP-9 production. In contrast, MMP-9 production was down-modulated when human macrophage cultures were treated with IFN-γ or IL-4 before infection. Human macrophages infected with T.cruzi Y or Colombian strains produced increased levels of MMP-9, which was related to the production of cytokines such as IL-1β, TNF-α and IL-6. © 2014.


Czaikoski P.G.,University of Sao Paulo | Menaldo D.L.,University of Sao Paulo | Marcussi S.,University of Sao Paulo | Baseggio A.L.C.,Laboratorio Of Imunologia Clinica | And 8 more authors.
Blood Coagulation and Fibrinolysis | Year: 2010

Previous studies have shown that venoms of social wasps and bees exhibit strong anticoagulant activity. The present study describes the anticoagulant and fibrinogen-degrading pharmacological properties of the venom of Polybia occidentalis social wasp. The results demonstrated that this venom presented anticoagulant effect, inhibiting the coagulation at different steps of the clotting pathway (intrinsic, extrinsic and common pathway). The venom inhibited platelet aggregation and degraded plasma fibrinogen, possibly containing metal-dependent metalloproteases that specifically cleave the Bβ-chain of fibrinogen. In conclusion, fibrinogenolytic and anticoagulant properties of this wasp venom find a potential application in drug development for the treatment of thrombotic disorders. For that, further studies should be carried out in order to identify and isolate the active compounds responsible for these effects. © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins.


Urbaczek A.C.,Laboratorio Of Imunologia Clinica | De Abreu Ribeiro L.C.,Laboratorio Of Imunologia Clinica | Ximenes V.F.,São Paulo State University | Afonso A.,New University of Lisbon | And 9 more authors.
Memorias do Instituto Oswaldo Cruz | Year: 2014

The hepatitis C virus (HCV) encodes approximately 10 different structural and non-structural proteins, including the envelope glycoprotein 2 (E2). HCV proteins, especially the envelope proteins, bind to cell receptors and can damage tissues. Endothelial inflammation is the most important determinant of fibrosis progression and, consequently, cirrhosis. The aim of this study was to evaluate and compare the inflammatory response of endothelial cells to two recombinant forms of the HCV E2 protein produced in different expression systems (Escherichia coli and Pichia pastoris). We observed the induction of cell death and the production of nitric oxide, hydrogen peroxide, interleukin-8 and vascular endothelial growth factor A in human umbilical vein endothelial cells (HUVECs) stimulated by the two recombinant E2 proteins. The E2-induced apoptosis of HUVECs was confirmed using the molecular marker PARP. The apoptosis rescue observed when the antioxidant N-acetylcysteine was used suggests that reactive oxygen species are involved in E2-induced apoptosis. We propose that these proteins are involved in the chronic inflammation caused by HCV. © 2014 Fundacao Oswaldo Cruz. All rights reserved.


PubMed | Federal University of São Carlos, University of Sao Paulo, São Paulo State University, Laboratorio Of Imunologia Clinica and New University of Lisbon
Type: | Journal: Memorias do Instituto Oswaldo Cruz | Year: 2014

The hepatitis C virus (HCV) encodes approximately 10 different structural and non-structural proteins, including the envelope glycoprotein 2 (E2). HCV proteins, especially the envelope proteins, bind to cell receptors and can damage tissues. Endothelial inflammation is the most important determinant of fibrosis progression and, consequently, cirrhosis. The aim of this study was to evaluate and compare the inflammatory response of endothelial cells to two recombinant forms of the HCV E2 protein produced in different expression systems (Escherichia coli and Pichia pastoris). We observed the induction of cell death and the production of nitric oxide, hydrogen peroxide, interleukin-8 and vascular endothelial growth factor A in human umbilical vein endothelial cells (HUVECs) stimulated by the two recombinant E2 proteins. The E2-induced apoptosis of HUVECs was confirmed using the molecular marker PARP. The apoptosis rescue observed when the antioxidant N-acetylcysteine was used suggests that reactive oxygen species are involved in E2-induced apoptosis. We propose that these proteins are involved in the chronic inflammation caused by HCV.


PubMed | Federal University of São Carlos, University of Sao Paulo, São Paulo State University, Laboratorio Of Imunologia Clinica and New University of Lisbon
Type: Journal Article | Journal: Memorias do Instituto Oswaldo Cruz | Year: 2014

The hepatitis C virus (HCV) encodes approximately 10 different structural and non-structural proteins, including the envelope glycoprotein 2 (E2). HCV proteins, especially the envelope proteins, bind to cell receptors and can damage tissues. Endothelial inflammation is the most important determinant of fibrosis progression and, consequently, cirrhosis. The aim of this study was to evaluate and compare the inflammatory response of endothelial cells to two recombinant forms of the HCV E2 protein produced in different expression systems (Escherichia coli and Pichia pastoris). We observed the induction of cell death and the production of nitric oxide, hydrogen peroxide, interleukin-8 and vascular endothelial growth factor A in human umbilical vein endothelial cells (HUVECs) stimulated by the two recombinant E2 proteins. The E2-induced apoptosis of HUVECs was confirmed using the molecular marker PARP. The apoptosis rescue observed when the antioxidant N-acetylcysteine was used suggests that reactive oxygen species are involved in E2-induced apoptosis. We propose that these proteins are involved in the chronic inflammation caused by HCV.


PubMed | Laboratorio Of Imunologia Clinica
Type: | Journal: Journal of inflammation (London, England) | Year: 2015

Tuberculosis (TB) is the second greatest killer worldwide that is caused by a single infectious agent. For its control, studies of TB vaccines are needed. Since Bacillus Calmette-Guerin (BCG) is the only vaccine against TB currently in use, studies addressing the protective role of BCG in the context of inducible inflammatory mediators are urgently required.In this study, groups of HIV-negative adult healthy donors (HD; n=42) and neonates (UV; n=18) have been voluntarily enrolled, and BCG Moreau strain was used for the in vitro mononuclear cell infections for an initial period of 48h. Subsequently, harvested conditioned medium (CM) was added to autologous resting cells for an additional 24, 48, and 120h, and Annexin V, in conjunction with a vital dye, was then used for apoptosis detection. CM was also assayed for nitric oxide (NO), prostaglandin E2 (PGE2), leukotriene B4 (LTB4), interferon (IFN)-, and transforming growth factor (TGF)-1 levels. The p values were set up for any differences between two groups of individuals using Students t-test and considered significant when0.05.At 120h, CM induced the highest apoptosis levels in both group studied, but necrosis was high in UV group only (p-value<0.05). NO was released equally during BCG infection in both groups, but higher levels were found in HD when compared with UV group (p-value<0.05). Overall, BCG Moreau triggered high PGE2, LTB4 and IFN- productions in macrophages from the UV group (p-value0.05), whereas the prostanoid PGE2 and TGF-1 had an opposite pattern in the HD group.This study uncovers critical roles for endogenous compounds in the instruction of host macrophage cell death patterns. Understanding the regulation of human immune responses is critical for vaccine development and the treatment of infectious diseases. These findings shed new light on the potential condition for a booster immunization in individuals already vaccinated with BCG for TB protection, and further studies are warranted.

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