José O. Previato

Universidade Federal do Rio de Janeiro

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Lúcia Mendonça‐Previato

Universidade Federal do Rio de Janeiro

144

Leonardo Freire‐de‐Lima

Universidade Federal do Rio de Janeiro

Célio Geraldo Freire-de-Lima

Universidade Federal do Rio de Janeiro

Christopher Jones

Center for Drug Evaluation and Research

Leonardo Marques da Fonseca

Universidade Federal do Rio de Janeiro

Adriane R. Todeschini

Universidade Federal do Rio de Janeiro

Kelli Monteiro da Costa

Universidade Federal do Rio de Janeiro

Alexandre Morrot

Universidade Federal do Rio de Janeiro

Robin Wait

Imperial College London

Débora Decoté‐Ricardo

Universidade Federal Rural do Rio de Janeiro

Cooperative Institutions

Universidade Federal do Rio de Janeiro

210

Bial (Portugal)

176

Harvard University

University of California, San Diego

Centre National de la Recherche Scientifique

National Institutes of Health

Fundação Oswaldo Cruz

Fundação Carlos Chagas Filho de Amparo à Pesquisa do Estado do Rio de Janeiro

Instituto de Biofísica Carlos Chagas Filho

University of Georgia

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Heterogeneity in the Biosynthesis of Mucin O-Glycans from Trypanosoma cruzi Tulahuen Strain with the Expression of Novel Galactofuranosyl-Containing Oligosaccharides

Biochemistry (2004)

Christopher Jones Adriane R. Todeschini Orlando A. Agrellos José O. Previato Lúcia Mendonça‐Previato

Sialoglycoprotein from Trypanosoma cruzi strains participates in important biological functions in which the O-linked glycans play a pivotal role, and their structural diversity may be related to the parasite's virulence pattern. To provide supporting evidence for this idea, we have determined the structure of novel linear and branched α-O-GlcNAc-linked oligosaccharides present on the mucins of the T. cruzi Tulahuen strain. The O-glycans were isolated as oligosaccharide alditols by reductive β-elimination, purified, and characterized by nuclear magnetic resonance spectroscopy and methylation analysis. Two core families were synthesized by the parasite: the Galfβ1→4GlcNAc and Galpβ1→4GlcNAc. The Galfβ1→4GlcNAc core yields three series of O-chain structures. In the first, the Galf residue is nonsubstituted, while in the other series it is elongated by the activity of galactopyranosyl or galactofuranosyl transferases giving rise to Galp-β-(1→2)-Galf-β-(1→4) or Galf-β-(1→2)-Galf-β-(1→4) substructures not previously observed. The three series can arise by further galactopyranosylation of the GlcNAc O-6 arm. Sialylation was the only observed elaboration of the Galpβ1→4GlcNAc core family. Thus the determination of the structures of the O-glycans from T. cruzi Tulahuen mucins confirms the strain specificity of the glycosylation and predicts a relationship between it and parasite pathogenicity and the epidemiology of Chagas' disease.

Oligosaccharide

Strain (injury)

Chagas Disease

10.1021/bi048942u

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Citations (50)

Intrinsic and Chemotherapeutic Stressors Modulate ABCC-Like Transport in Trypanosoma cruzi

Molecules (2021)

Kelli Monteiro da Costa Eduardo J. Salustiano Raphael do Carmo Valente Leonardo Freire‐de‐Lima Lúcia Mendonça‐Previato

Trypanosoma cruzi is the etiologic agent for Chagas disease, which affects 6–7 million people worldwide. The biological diversity of the parasite reflects on inefficiency of benznidazole, which is a first choice chemotherapy, on chronic patients. ABC transporters that extrude xenobiotics, metabolites, and mediators are overexpressed in resistant cells and contribute to chemotherapy failure. An ABCC-like transport was identified in the Y strain and extrudes thiol-conjugated compounds. As thiols represent a line of defense towards reactive species, we aimed to verify whether ABCC-like transport could participate in the regulation of responses to stressor stimuli. In order to achieve this, ABCC-like activity was measured by flow cytometry using fluorescent substrates. The present study reveals the participation of glutathione and ceramides on ABCC-like transport, which are both implicated in stress. Hemin modulated the ABCC-like efflux which suggests that this protein might be involved in cellular detoxification. Additionally, all strains evaluated exhibited ABCC-like activity, while no ABCB1-like activity was detected. Results suggest that ABCC-like efflux is not associated with natural resistance to benznidazole, since sensitive strains showed higher activity than the resistant ones. Although benznidazole is not a direct substrate, ABCC-like efflux increased after prolonged drug exposure and this indicates that the ABCC-like efflux mediated protection against cell stress depends on the glutathione biosynthesis pathway.

Benznidazole

Efflux

10.3390/molecules26123510

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Citations (2)

Correction to: Expression of O-glycosylated oncofetal fibronectin in alternatively activated human macrophages

Immunologic Research (2022)

Marcos André Rodrigues da Costa Santos Jhenifer Santos dos Reis Carlos Antônio do Nascimento Santos Kelli Monteiro da Costa Pedro Marçal Barcelos

Oncofetal antigen

Expression (computer science)

10.1007/s12026-022-09338-0

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Citations (0)

Structural variation in the glycoinositolphospholipids of different strains ofTrypanosoma cruzi

Glycoconjugate Journal (1996)

Jo�o C. Carreira Christopher Jones Robin Wait José O. Previato Lúcia Mendonça‐Previato

Moiety

Strain (injury)

Oligosaccharide

10.1007/bf01053191

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Citations (70)

Glycoinositolphospholipid from Trypanosoma cruzi: Structure, Biosynthesis and Immunobiology

Advances in Parasitology/Advances in parasitology (2003)

José O. Previato Robin Wait Christopher Jones George A. DosReis Adriane R. Todeschini

Chagas Disease

Protozoan parasite

10.1016/s0065-308x(03)56001-8

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Citations (76)

X-linked immunodeficient (XID) mice exhibit high susceptibility to Cryptococcus gattii infection

Scientific Reports (2021)

Israel Diniz-Lima Pablo Rodrigo da Rosa Elias Barbosa da Silva-Júnior Joyce Cristina Guimarães-de-Oliveira Elisângela Oliveira de Freitas

Abstract Cryptococcosis is an opportunistic disease caused by the fungus Cryptococcus neoformans and Cryptococcus gattii . It starts as a pulmonary infection that can spread to other organs, such as the brain, leading to the most serious occurrence of the disease, meningoencephalitis. The humoral response has already been described in limiting the progression of cryptococcosis where the B-1 cell seems to be responsible for producing natural IgM antibodies, crucial for combating fungal infections. The role of the B-1 cell in C. neoformans infection has been initially described, however the role of the humoral response of B-1 cells has not yet been evaluated during C. gattii infections. In the present study we tried to unravel this issue using XID mice, a murine model deficient in the Btk protein which compromises the development of B-1 lymphocytes. We use the XID mice compared to BALB/c mice that are sufficient for the B-1 population during C. gattii infection. Our model of chronic lung infection revealed that XID mice, unlike the sufficient group of B-1, had early mortality with significant weight loss, in addition to reduced levels of IgM and IgG specific to GXM isolated from the capsule of C. neoformans . In addition to this, we observed an increased fungal load in the blood and in the brain. We described an increase in the capsular size of C. gattii and the predominant presence of cytokines with a Th2 profile was also observed in these animals. Thus, the present study strongly points to a higher susceptibility of the XID mouse to C. gattii , which suggests that the presence of B-1 cells and anti-GXM antibodies is fundamental during the control of infection by C. gattii .

Cryptococcus gattii

Humoral immunity

10.1038/s41598-021-97041-9

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Citations (8)

Primary structure of the oligosaccharide chain of lipopeptidophosphoglycan of epimastigote forms of Trypanosoma cruzi.

Journal of Biological Chemistry (1990)

José O. Previato Philip A.J. Gorin Mytosk Mazurek Márcia Tosta Xavier Bernard Fournet

The lipopeptidophosphoglycan of epimastigote forms of Trypanosoma cruzi is composed of a glycan linked through a non-N-acetylated glucosamine residue to an inositol phosphorylceramide. Using conventional analysis techniques, including 1H, 13C, and 31P NMR spectroscopy and negative ion fast atom bombardment mass spectroscopy, the structure of the carbohydrate-containing part of the molecule is determined as: (Sequence: see text). There is uncertainty as to which 2-O-substituted alpha-D-Manp unit is attached the side chain or whether it is distributed between the two units. Some of the structures lack the Galf side chain. The inositol unit is linked to ceramide via a phosphodiester bridge. The major aliphatic components of the ceramide portion were lignoceric acid and sphinganine.

Side chain

Protein primary structure

Sphingolipid

Phosphodiester bond

Residue (chemistry)

10.1016/s0021-9258(19)39831-x

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Citations (149)

Modulation of B-Lymphocyte and NK Cell Activities by Glycoinositolphospholipid Purified fromTrypanosoma cruzi

Infection and Immunity (1999)

Luciana Barros de Arruda Lúcia Mendonça‐Previato José O. Previato Quirijn Vos James J. Mond

ABSTRACT Glycoinositolphospholipids (GIPLs) are some of the major glycolipids of the Trypanosoma cruzi surface that were previously shown to activate B cells. In the present study, we investigated whether (i) T. cruzi GIPLs could induce immunoglobulin secretion from B cells in the absence of T cells and NK cells and whether (ii) NK cells are also stimulated by the GIPLs. B cells purified from mice deficient in both T and NK cells (CD3ɛ transgenic mice) secreted immunoglobulin in response to the GIPL. This response was increased by coculture with a murine NK cell line. The T. cruzi GIPL also increased the NK cell (interleukin-2 induced) proliferative response. Our data indicate that the T. cruzi GIPL has a direct stimulatory effect on NK cells and induces immunoglobulin secretion in the absence of T lymphocytes and NK cells. These findings suggest that this T. cruzi -derived molecule may be one of the stimulators that lead to NK cell activation during T. cruzi infection.

10.1128/iai.67.11.6177-6180.1999

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Citations (16)

Expression of O-glycosylated oncofetal fibronectin in alternatively activated human macrophages

Immunologic Research (2022)

Marcos André Rodrigues da Costa Santos Jhenifer Santos dos Reis Carlos Antônio do Nascimento Santos Kelli Monteiro da Costa Pedro Marçal Barcelos

10.1007/s12026-022-09321-9

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Citations (11)

Proinflammatory and Cytotoxic Effects of Hexadecylphosphocholine (Miltefosine) against Drug-Resistant Strains of Trypanosoma cruzi

Antimicrobial Agents and Chemotherapy (2002)

Víctor Barbosa Saraiva Daniel Gibaldi José O. Previato Lúcia Mendonça‐Previato Marcelo T. Bozza

ABSTRACT The increased resistance of the protozoan parasite Trypanosoma cruzi to nitro derivatives is one of the major problems for the successful treatment of Chagas' disease. In the present study, we have tested the effects of 1- O -hexadecylphosphocholine (miltefosine) against strains of T. cruzi that are partially resistant (strain Y) and highly resistant (strain Colombiana) to the drugs in clinical use. As expected, epimastigotes of strain Colombiana showed higher levels of resistance to benznidazole than those of strain Y. However, the level of resistance to miltefosine was the same for both strains. This alkylphospholipid was also extremely toxic against intracellular amastigotes of both strains. This ether-lipid analogue induced in a dose-dependent manner the production of tumor necrosis factor alpha and nitric oxide (NO) radicals by infected and noninfected macrophages, suggesting that miltefosine may activate macrophages in vitro. Nevertheless, the cytotoxic effect of miltefosine against intracellular amastigotes was independent of the amount of NO produced by the infected macrophages since the same dose-response curves for miltefosine were observed when the NO production was blocked by the NO synthase inhibitor N G -monomethyl- l -arginine monoacetate. Preliminary in vivo studies with BALB/c mice infected with strain Y indicated that oral miltefosine promoted survival and reduced the parasitemia to levels comparable to those observed when benznidazole was used. Four months after treatment, no parasites were detected in the blood or spleen tissue sections maintained in culture. Together, these results support the hypothesis that miltefosine may be used for the treatment of Chagas' disease, including cases caused by resistant strains of T. cruzi .

Miltefosine

Benznidazole

Amastigote

10.1128/aac.46.11.3472-3477.2002

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Citations (51)