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Pedro L. Oliveira

Other affiliations: Johns Hopkins University
Bio: Pedro L. Oliveira is an academic researcher from Federal University of Rio de Janeiro. The author has contributed to research in topics: Rhodnius prolixus & Heme. The author has an hindex of 44, co-authored 112 publications receiving 5565 citations. Previous affiliations of Pedro L. Oliveira include Johns Hopkins University.
Topics: Rhodnius prolixus, Heme, Hemolymph, Midgut, Hemozoin


Papers
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Journal ArticleDOI
TL;DR: It is demonstrated that heme, but not its analogs/precursors, induced tumor necrosis factor-α (TNF-α) secretion by macrophages dependently on MyD88, TLR4, and CD14, and these findings support the concept that the broad ligand specificity ofTLR4 and the different activation profiles might in part reside in its ability to recognize different ligands in different binding sites.

492 citations

Journal ArticleDOI
Rafael D. Mesquita1, Raquel J. Vionette-Amaral1, Carl Lowenberger2, Rolando Rivera-Pomar3, Fernando A. Monteiro4, Fernando A. Monteiro1, Patrick Minx5, John Spieth5, A. Bernardo Carvalho1, Francisco Panzera6, Daniel Lawson7, André Q. Torres1, André Q. Torres4, José M. C. Ribeiro8, Marcos Henrique Ferreira Sorgine1, Robert M. Waterhouse, Michael J. Montague5, Fernando Abad-Franch4, Michele Alves-Bezerra1, Laurence Rodrigues do Amaral9, Helena Araujo1, Ricardo Nascimento Araújo10, Ricardo Nascimento Araújo1, L. Aravind8, Georgia C. Atella1, Patrícia Azambuja4, Patrícia Azambuja1, Mateus Berni1, Paula R. Bittencourt-Cunha1, Glória R.C. Braz1, Gustavo M. Calderón-Fernández3, Claudia M. A. Carareto11, Mikkel B. Christensen7, Igor Rodrigues da Costa1, Samara G. da Costa4, Marilvia Dansa12, Carlos R. O. Daumas-Filho1, Iron F. De-Paula1, Felipe A. Dias1, George Dimopoulos13, Scott J. Emrich14, Natalia Esponda-Behrens3, Patrícia Fampa15, Rita D. Fernandez-Medina4, Rodrigo Nunes da Fonseca1, Marcio Fontenele1, Catrina Fronick5, Lucinda Fulton5, Ana Caroline P. Gandara1, Eloi S. Garcia1, Eloi S. Garcia4, Fernando A. Genta4, Fernando A. Genta1, Gloria I. Giraldo-Calderón14, Bruno Gomes4, Bruno Gomes1, Katia C. Gondim1, Adriana Granzotto11, Alessandra A. Guarneri1, Alessandra A. Guarneri4, Roderic Guigó16, Myriam Harry17, Daniel S.T. Hughes7, Willy Jablonka1, Emmanuelle Jacquin-Joly, M. Patricia Juárez3, Leonardo Koerich1, Angela B. Lange18, Jose Manuel Latorre-Estivalis1, Jose Manuel Latorre-Estivalis4, Andrés Lavore3, Gena G. Lawrence19, Gena G. Lawrence18, Cristiano Lazoski1, Claudio R. Lazzari17, Raphael R.S. Lopes1, Marcelo G. Lorenzo1, Marcelo G. Lorenzo4, Magda D. Lugon12, David Majerowicz1, Paula L. Marcet19, Marco Mariotti16, Hatisaburo Masuda1, Karyn Megy7, Ana C.A. Melo1, Fanis Missirlis20, Theo Mota10, Fernando G. Noriega21, Marcela Nouzova21, Rodrigo Dutra Nunes1, Raquel L.L. Oliveira1, Gilbert Oliveira-Silveira1, Sheila Ons3, Ian Orchard18, Lucia Pagola3, Gabriela O. Paiva-Silva1, Agustina Pascual3, Márcio G. Pavan4, Nicolás Pedrini3, Alexandre A. Peixoto1, Alexandre A. Peixoto4, Marcos H. Pereira1, Marcos H. Pereira10, Andrew Pike13, Carla Polycarpo1, Francisco Prosdocimi1, Rodrigo Ribeiro-Rodrigues22, Hugh M. Robertson23, Ana Paula Salerno, Didier Salmon1, Didac Santesmasses16, Renata Schama1, Renata Schama4, Eloy S. Seabra-Junior, Lívia Silva-Cardoso1, Mário A.C. Silva-Neto1, Matheus Souza-Gomes9, Marcos Sterkel1, Mabel L. Taracena1, Marta Tojo24, Zhijian Jake Tu25, Jose M. C. Tubio26, Raul Ursic-Bedoya2, Thiago M. Venancio12, Thiago M. Venancio1, Ana Beatriz Walter-Nuno1, Derek Wilson7, Wesley C. Warren5, Richard K. Wilson5, Erwin Huebner27, Ellen M. Dotson19, Pedro L. Oliveira1 
TL;DR: The first genome sequence of a nondipteran insect vector of an important human parasitic disease is described, which provides critical information on the physiology and evolution of this important vector species and should be instrumental for the development of innovative disease control methods.
Abstract: Rhodnius prolixus not only has served as a model organism for the study of insect physiology, but also is a major vector of Chagas disease, an illness that affects approximately seven million people worldwide. We sequenced the genome of R. prolixus, generated assembled sequences covering 95% of the genome (∼ 702 Mb), including 15,456 putative protein-coding genes, and completed comprehensive genomic analyses of this obligate blood-feeding insect. Although immune-deficiency (IMD)-mediated immune responses were observed, R. prolixus putatively lacks key components of the IMD pathway, suggesting a reorganization of the canonical immune signaling network. Although both Toll and IMD effectors controlled intestinal microbiota, neither affected Trypanosoma cruzi, the causal agent of Chagas disease, implying the existence of evasion or tolerance mechanisms. R. prolixus has experienced an extensive loss of selenoprotein genes, with its repertoire reduced to only two proteins, one of which is a selenocysteine-based glutathione peroxidase, the first found in insects. The genome contained actively transcribed, horizontally transferred genes from Wolbachia sp., which showed evidence of codon use evolution toward the insect use pattern. Comparative protein analyses revealed many lineage-specific expansions and putative gene absences in R. prolixus, including tandem expansions of genes related to chemoreception, feeding, and digestion that possibly contributed to the evolution of a blood-feeding lifestyle. The genome assembly and these associated analyses provide critical information on the physiology and evolution of this important vector species and should be instrumental for the development of innovative disease control methods.

293 citations

Journal ArticleDOI
TL;DR: In this paper, the authors review mechanisms by which heme can exert biological damage, together with a wide spectrum of adaptations developed by blood-feeding insects and ticks to counteract its deleterious effects.

293 citations

Journal ArticleDOI
01 Jun 2002-Blood
TL;DR: A role for hemin as a proinflammatory agent able to induce polymorphonuclear neutrophil activation in situations of clinical relevance, such as hemolysis or hemoglobinemia is suggested.

263 citations

Journal ArticleDOI
TL;DR: It is proposed that a controlled decrease in ROS levels in the midgut of Aedes aegypti is an adaptation to compensate for the ingestion of heme, a pro-oxidant molecule released in large amounts upon hemoglobin degradation, which would represent a burden to the insect.
Abstract: The presence of bacteria in the midgut of mosquitoes antagonizes infectious agents, such as Dengue and Plasmodium, acting as a negative factor in the vectorial competence of the mosquito. Therefore, knowledge of the molecular mechanisms involved in the control of midgut microbiota could help in the development of new tools to reduce transmission. We hypothesized that toxic reactive oxygen species (ROS) generated by epithelial cells control bacterial growth in the midgut of Aedes aegypti, the vector of Yellow fever and Dengue viruses. We show that ROS are continuously present in the midgut of sugar-fed (SF) mosquitoes and a blood-meal immediately decreased ROS through a mechanism involving heme-mediated activation of PKC. This event occurred in parallel with an expansion of gut bacteria. Treatment of sugar-fed mosquitoes with increased concentrations of heme led to a dose dependent decrease in ROS levels and a consequent increase in midgut endogenous bacteria. In addition, gene silencing of dual oxidase (Duox) reduced ROS levels and also increased gut flora. Using a model of bacterial oral infection in the gut, we show that the absence of ROS resulted in decreased mosquito resistance to infection, increased midgut epithelial damage, transcriptional modulation of immune-related genes and mortality. As heme is a pro-oxidant molecule released in large amounts upon hemoglobin degradation, oxidative killing of bacteria in the gut would represent a burden to the insect, thereby creating an extra oxidative challenge to the mosquito. We propose that a controlled decrease in ROS levels in the midgut of Aedes aegypti is an adaptation to compensate for the ingestion of heme.

228 citations


Cited by
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01 Jun 2012
TL;DR: SPAdes as mentioned in this paper is a new assembler for both single-cell and standard (multicell) assembly, and demonstrate that it improves on the recently released E+V-SC assembler and on popular assemblers Velvet and SoapDeNovo (for multicell data).
Abstract: The lion's share of bacteria in various environments cannot be cloned in the laboratory and thus cannot be sequenced using existing technologies. A major goal of single-cell genomics is to complement gene-centric metagenomic data with whole-genome assemblies of uncultivated organisms. Assembly of single-cell data is challenging because of highly non-uniform read coverage as well as elevated levels of sequencing errors and chimeric reads. We describe SPAdes, a new assembler for both single-cell and standard (multicell) assembly, and demonstrate that it improves on the recently released E+V-SC assembler (specialized for single-cell data) and on popular assemblers Velvet and SoapDeNovo (for multicell data). SPAdes generates single-cell assemblies, providing information about genomes of uncultivatable bacteria that vastly exceeds what may be obtained via traditional metagenomics studies. SPAdes is available online ( http://bioinf.spbau.ru/spades ). It is distributed as open source software.

10,124 citations

Journal ArticleDOI
06 Apr 2005-JAMA
TL;DR: A growing body of evidence supports the existence of a novel mechanism of human disease, namely, hemolysis-associated smooth muscle dystonia, vasculopathy, and endothelial dysfunction.
Abstract: ContextThe efficient sequestration of hemoglobin by the red blood cell membrane and the presence of multiple hemoglobin clearance mechanisms suggest a critical need to prevent the buildup of this molecule in the plasma. A growing list of clinical manifestations attributed to hemoglobin release in a variety of acquired and iatrogenic hemolytic disorders suggests that hemolysis and hemoglobinemia should be considered as a novel mechanism of human disease.Evidence AcquisitionPertinent scientific literature databases and references were searched through October 2004 using terms that encompassed various aspects of hemolysis, hemoglobin preparations, clinical symptoms associated with plasma hemoglobin, nitric oxide in hemolysis, anemia, pulmonary hypertension, paroxysmal nocturnal hemoglobinuria, and sickle-cell disease.Evidence SynthesisHemoglobin is released into the plasma from the erythrocyte during intravascular hemolysis in hereditary, acquired, and iatrogenic hemolytic conditions. When the capacity of protective hemoglobin-scavenging mechanisms has been saturated, levels of cell-free hemoglobin increase in the plasma, resulting in the consumption of nitric oxide and clinical sequelae. Nitric oxide plays a major role in vascular homeostasis and has been shown to be a critical regulator of basal and stress-mediated smooth muscle relaxation and vasomotor tone, endothelial adhesion molecule expression, and platelet activation and aggregation. Thus, clinical consequences of excessive cell-free plasma hemoglobin levels during intravascular hemolysis or the administration of hemoglobin preparations include dystonias involving the gastrointestinal, cardiovascular, pulmonary, and urogenital systems, as well as clotting disorders. Many of the clinical sequelae of intravascular hemolysis in a prototypic hemolytic disease, paroxysmal nocturnal hemoglobinuria, are readily explained by hemoglobin-mediated nitric oxide scavenging.ConclusionA growing body of evidence supports the existence of a novel mechanism of human disease, namely, hemolysis-associated smooth muscle dystonia, vasculopathy, and endothelial dysfunction.

1,370 citations

Journal ArticleDOI
TL;DR: In this paper, the authors show that the activation of HO-1 is an ubiquitous cellular response to oxidative stress, and that the reaction products of HO activity, biliverdin, and its subsequent metabolite bilirubin, have antioxidant properties.

781 citations

Journal ArticleDOI
TL;DR: Free heme acts as a pro-inflammatory molecule and heme-induced inflammation is involved in the pathology of diverse conditions; such as renal failure, arteriosclerosis, and complications after artificial blood transfusion, peritoneal endometriosis, and heart transplant failure.

746 citations