Anderson Guimaraes Baptista Costa

@microbiologia.ufrj.br

Professor/ Immunology/Microbiology Institute
Federal University of Rio de Janeiro

Anderson Guimaraes Baptista Costa


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https://researchid.co/anderson.guimaraes

RESEARCH, TEACHING, or OTHER INTERESTS

Immunology, Microbiology
23

Scopus Publications

Scopus Publications

  • Correction: Gene deletion as a possible strategy adopted by New World Leishmania infantum to maximize geographic dispersion (PLOS Pathogens (2025) 21:3 (e1012938) DOI: 10.1371/journal.ppat.1012938)
    Monique Florêncio, Marne Coimbra Batalha Chagas, Anderson Guimarães-Costa, Jullyanna Oliveira, Ingrid Waclawiak, Thamara K. F. Oliveira, Elvira Maria Saraiva, Anita Leocadio Freitas-Mesquita, José Roberto Meyer-Fernandes, Laura Aragão-Farias, Camilly Enes Trindade, Patricia Cuervo, Renata Azevedo do Nascimento, Otacilio C. Moreira, Flávia Lima Ribeiro-Gomes, Yara M. Traub-Csekö, Erich Loza Telleria, Slavica Vaselek, Tereza Leštinová, Petr Volf, Gerald F. Späth, Elisa Cupolillo, Mariana Côrtes Boité
    Plos Pathogens, 2025
    [This corrects the article DOI: 10.1371/journal.ppat.1012938.].
  • Gene deletion as a possible strategy adopted by New World Leishmania infantum to maximize geographic dispersion
    Monique Florêncio, Marne Coimbra Batalha Chagas, Anderson Guimarães-Costa, Jullyanna Oliveira, Ingrid Waclawiak, Thamara K. F. Oliveira, Elvira Maria Saraiva, Anita Leocadio Freitas-Mesquita, José Roberto Meyer-Fernandes, Laura Aragão-Farias, Camilly Enes Trindade, Patricia Cuervo, Renata Azevedo do Nascimento, Otacilio C. Moreira, Flávia Lima Ribeiro-Gomes, Yara M. Traub-Csekö, Erich Loza Telleria, Slavica Vaselek, Tereza Leštinová, Petr Volf, Gerald F. Späth, Elisa Cupolillo, Mariana Côrtes Boité
    Plos Pathogens, 2025
    Background The present study investigates implications of a sub-chromosomal deletion in Leishmania infantum strains, the causative agent of American Visceral Leishmaniasis (AVL). Primarily found in New World strains, the deletion leads to the absence of the ecto-3’-nucleotidase/nuclease enzyme, impacting parasite virulence, pathogenicity, and drug susceptibility. The factors favoring prevalence and the widespread geographic distribution of these deleted mutant parasites (DEL) in the NW (NW) are discussed under the generated data. Methods We conducted phenotypic assessments of the sub-chromosomal deletion through in vitro assays with axenic parasites and experimental infections in both in vitro and in vivo models of vertebrate and invertebrate hosts using geographically diverse mutant field isolates. Results Despite reduced pathogenicity, the DEL strains efficiently infect vertebrate hosts and exhibit relevant differences, including enhanced metacyclogenesis and colonization rates in sand flies, potentially facilitating transmission. This combination may represent a more effective way to maintain and disperse the transmission cycle of DEL strains. Conclusions Phenotypic assessments reveal altered parasite fitness, with potential enhanced transmissibility at the population level. Reduced susceptibility of DEL strains to miltefosine, a key drug in VL treatment, further complicates control efforts. The study underscores the importance of typing parasite genomes for surveillance and control, advocating for the sub-chromosomal deletion as a molecular marker in AVL management.
  • Leishmania infantum Axenic Amastigotes Induce Human Neutrophil Extracellular Traps and Resist NET-Mediated Killing
    Thamara K. F. Oliveira, Jullyanna Oliveira-Silva, Leandra Linhares-Lacerda, Vanderlei da Silva Fraga-Junior, Claudia F. Benjamim, Anderson B. Guimaraes-Costa, Elvira M. Saraiva
    Tropical Medicine and Infectious Disease, 2023
    Neutrophils are multifaceted cells that, upon activation, release meshes of chromatin associated with different proteins, known as neutrophil extracellular traps (NETs). Leishmania amazonensis promastigotes and amastigotes induce NET release, and we have identified the signaling pathways involved in NET extrusion activated by promastigotes. Amastigotes maintain the infection in vertebrate hosts, and we have shown the association of NETs with amastigotes in human biopsies of cutaneous leishmaniasis. However, the interaction of amastigotes and neutrophils remains poorly understood. Our study aimed to characterize the pathways involved in the formation of NETs induced by axenic amastigotes from L. infantum, the causal agent of visceral leishmaniasis. Human neutrophils pretreated with signaling pathway inhibitors were incubated with amastigotes, and NET release was quantified in the culture supernatant. Amastigote viability was checked after incubation with NETs. We found that the release of NETs by neutrophils stimulated with these amastigotes requires the participation of elastase and peptidyl arginine deaminase and the involvement of PI3K, ROS, and calcium. Moreover, amastigotes are not susceptible to NET-mediated killing. Altogether, these findings improve our comprehension of the signaling pathways implicated in the interaction between amastigotes and human neutrophils.
  • A sand fly salivary protein acts as a neutrophil chemoattractant
    Anderson B. Guimaraes-Costa, John P. Shannon, Ingrid Waclawiak, Jullyanna Oliveira, Claudio Meneses, Waldione de Castro, Xi Wen, Joseph Brzostowski, Tiago D. Serafim, John F. Andersen, Heather D. Hickman, Shaden Kamhawi, Jesus G. Valenzuela, Fabiano Oliveira
    Nature Communications, 2021
    Apart from bacterial formyl peptides or viral chemokine mimicry, a non-vertebrate or insect protein that directly attracts mammalian innate cells such as neutrophils has not been molecularly characterized. Here, we show that members of sand fly yellow salivary proteins induce in vitro chemotaxis of mouse, canine and human neutrophils in transwell migration or EZ-TAXIScan assays. We demonstrate murine neutrophil recruitment in vivo using flow cytometry and two-photon intravital microscopy in Lysozyme-M-eGFP transgenic mice. We establish that the structure of this ~ 45 kDa neutrophil chemotactic protein does not resemble that of known chemokines. This chemoattractant acts through a G-protein-coupled receptor and is dependent on calcium influx. Of significance, this chemoattractant protein enhances lesion pathology (P < 0.0001) and increases parasite burden (P < 0.001) in mice upon co-injection with Leishmania parasites, underlining the impact of the sand fly salivary yellow proteins on disease outcome. These findings show that some arthropod vector-derived factors, such as this chemotactic salivary protein, activate rather than inhibit the host innate immune response, and that pathogens take advantage of these inflammatory responses to establish in the host.
  • Immunity to vector saliva is compromised by short sand fly seasons in endemic regions with temperate climates
    Fabiano Oliveira, Ekaterina Giorgobiani, Anderson B. Guimarães-Costa, Maha Abdeladhim, James Oristian, Lamzira Tskhvaradze, Nikoloz Tsertsvadze, Mariam Zakalashvili, Jesus G. Valenzuela, Shaden Kamhawi
    Scientific Reports, 2020
    Individuals exposed to sand fly bites develop humoral and cellular immune responses to sand fly salivary proteins. Moreover, cellular immunity to saliva or distinct salivary proteins protects against leishmaniasis in various animal models. In Tbilisi, Georgia, an endemic area for visceral leishmaniasis (VL), sand flies are abundant for a short period of ≤3 months. Here, we demonstrate that humans and dogs residing in Tbilisi have little immunological memory to saliva ofP. kandelakii, the principal vector of VL. Only 30% of humans and 50% of dogs displayed a weak antibody response to saliva after the end of the sand fly season. Likewise, their peripheral blood mononuclear cells mounted a negligible cellular immune response after stimulation with saliva. RNA seq analysis of wild-caughtP. kandelakiisalivary glands established the presence of a typical salivary repertoire that included proteins commonly found in other sand fly species such as the yellow, SP15 and apyrase protein families. This indicates that the absence of immunity toP. kandelakiisaliva in humans and dogs from Tbilisi is probably caused by insufficient exposure to sand fly bites. This absence of immunity to vector saliva will influence the dynamics of VL transmission in Tbilisi and other endemic areas with brief sand fly seasons.
  • Inflammatory profiling of patients with familial amyloid polyneuropathy
    Estefania P. Azevedo, Anderson B. Guimaraes-Costa, Christianne Bandeira-Melo, Leila Chimelli, Marcia Waddington-Cruz, Elvira M. Saraiva, Fernando L. Palhano, Debora Foguel
    BMC Neurology, 2019
    BACKGROUND: Familial amyloid polyneuropathy (FAP) or ATTRv (amyloid TTR variant) amyloidosis is a fatal hereditary disease characterized by the deposition of amyloid fibrils composed of transthyretin (TTR). The current diagnosis of ATTRv relies on genetic identification of TTR mutations and on Congo Red-positive amyloid deposits, which are absent in most ATTRv patients that are asymptomatic or early symptomatic, supporting the need for novel biomarkers to identify patients in earlier disease phases allowing disease control. METHODS: In an effort to search for new markers for ATTRv, our group searched for nine inflammation markers in ATTRv serum from a cohort of 28 Brazilian ATTRv patients. RESULTS: We found that the levels of six markers were increased (TNF-α, IL-1β, IL-8, IL-33, IFN-β and IL-10), one had decreased levels (IL-12) and two of them were unchanged (IL-6 and cortisol). Interestingly, asymptomatic patients already presented high levels of IL-33, IL-1β and IL-10, suggesting that inflammation may take place before fibril deposition. CONCLUSIONS: Our findings shed light on a new, previously unidentified aspect of ATTRv, which might help define new criteria for disease management, as well as provide additional understanding of ATTRv aggressiveness.
  • Human antibody reaction against recombinant salivary proteins of Phlebotomus orientalis in Eastern Africa
    Petra Sumova, Michal Sima, Tatiana Spitzova, Maha E. Osman, Anderson B. Guimaraes-Costa, Fabiano Oliveira, Dia-Eldin A. Elnaiem, Asrat Hailu, Alon Warburg, Jesus G. Valenzuela, Petr Volf
    Plos Neglected Tropical Diseases, 2018
    BACKGROUND: Phlebotomus orientalis is a vector of Leishmania donovani, the causative agent of life threatening visceral leishmaniasis spread in Eastern Africa. During blood-feeding, sand fly females salivate into the skin of the host. Sand fly saliva contains a large variety of proteins, some of which elicit specific antibody responses in the bitten hosts. To evaluate the exposure to sand fly bites in human populations from disease endemic areas, we tested the antibody reactions of volunteers' sera against recombinant P. orientalis salivary antigens. METHODOLOGY/PRINCIPAL FINDINGS: Recombinant proteins derived from sequence data on P. orientalis secreted salivary proteins, were produced using either bacterial (five proteins) or mammalian (four proteins) expression systems and tested as antigens applicable for detection of anti-P. orientalis IgG in human sera. Using these recombinant proteins, human sera from Sudan and Ethiopia, countries endemic for visceral leishmaniasis, were screened by ELISA and immunoblotting to identify the potential markers of exposure to P. orientalis bites. Two recombinant proteins; mAG5 and mYEL1, were identified as the most promising antigens showing high correlation coefficients as well as good specificity in comparison to the whole sand fly salivary gland homogenate. Combination of both proteins led to a further increase of correlation coefficients as well as both positive and negative predictive values of P. orientalis exposure. CONCLUSIONS/SIGNIFICANCE: This is the first report of screening human sera for anti-P. orientalis antibodies using recombinant salivary proteins. The recombinant salivary proteins mYEL1 and mAG5 proved to be valid antigens for screening human sera from both Sudan and Ethiopia for exposure to P. orientalis bites. The utilization of equal amounts of these two proteins significantly increased the capability to detect anti-P. orientalis antibody responses.
  • Immunity to LuloHya and Lundep, the salivary spreading factors from Lutzomyia longipalpis, protects against Leishmania major infection
    Ines Martin-Martin, Andrezza Campos Chagas, Anderson B. Guimaraes-Costa, Laura Amo, Fabiano Oliveira, Ian N. Moore, Thiago S. DeSouza-Vieira, Elda E. Sanchez, Montamas Suntravat, Jesus G. Valenzuela, Jose M. C. Ribeiro, Eric Calvo
    Plos Pathogens, 2018
    Salivary components from disease vectors help arthropods to acquire blood and have been shown to enhance pathogen transmission in different model systems. Here we show that two salivary enzymes from Lutzomyia longipalpis have a synergist effect that facilitates a more efficient blood meal intake and diffusion of other sialome components. We have previously shown that Lundep, a highly active endonuclease, enhances parasite infection and prevent blood clotting by inhibiting the intrinsic pathway of coagulation. To investigate the physiological role of a salivary hyaluronidase in blood feeding we cloned and expressed a recombinant hyaluronidase from Lu. longipalpis. Recombinant hyaluronidase (LuloHya) was expressed in mammalian cells and biochemically characterized in vitro. Our study showed that expression of neutrophil CXC chemokines and colony stimulating factors were upregulated in HMVEC cells after incubation with LuloHya and Lundep. These results were confirmed by the acute hemorrhage, edema and inflammation in a dermal necrosis (dermonecrotic) assay involving a massive infiltration of leukocytes, especially neutrophils, in mice co-injected with hemorrhagic factor and these two salivary proteins. Moreover, flow cytometry results showed that LuloHya and Lundep promote neutrophil recruitment to the bite site that may serve as a vehicle for establishment of Leishmania infection. A vaccination experiment demonstrated that LuloHya and Lundep confer protective immunity against cutaneous leishmaniasis using the Lu. longipalpis-Leishmania major combination as a model. Animals (C57BL/6) immunized with LuloHya or Lundep showed minimal skin damage while lesions in control animals remained ulcerated. This protective immunity was abrogated when B-cell-deficient mice were used indicating that antibodies against both proteins play a significant role for disease protection. Rabbit-raised anti-LuloHya antibodies completely abrogated hyaluronidase activity in vitro. Moreover, in vivo experiments demonstrated that blocking LuloHya with specific antibodies interferes with sand fly blood feeding. This work highlights the relevance of vector salivary components in blood feeding and parasite transmission and further suggests the inclusion of these salivary proteins as components for an anti-Leishmania vaccine.
  • Gut Microbes Egested during Bites of Infected Sand Flies Augment Severity of Leishmaniasis via Inflammasome-Derived IL-1β
    Ranadhir Dey, Amritanshu B. Joshi, Fabiano Oliveira, Lais Pereira, Anderson B. Guimarães-Costa, Tiago D. Serafim, Waldionê de Castro, Iliano V. Coutinho-Abreu, Parna Bhattacharya, Shannon Townsend, Hamide Aslan, Alec Perkins, Subir Karmakar, Nevien Ismail, Morgan Karetnick, Claudio Meneses, Robert Duncan, Hira L. Nakhasi, Jesus G. Valenzuela, Shaden Kamhawi
    Cell Host and Microbe, 2018
  • The Sand Fly Salivary Protein Lufaxin Inhibits the Early Steps of the Alternative Pathway of Complement by Direct Binding to the Proconvertase C3b-B
    Antonio F. Mendes-Sousa, Vladimir Fazito do Vale, Naylene C. S. Silva, Anderson B. Guimaraes-Costa, Marcos H. Pereira, Mauricio R. V. Sant’Anna, Fabiano Oliveira, Shaden Kamhawi, José M. C. Ribeiro, John F. Andersen, Jesus G. Valenzuela, Ricardo N. Araujo
    Frontiers in Immunology, 2017
    Saliva of the blood feeding sand fly Lutzomyia longipalpis was previously shown to inhibit the alternative pathway (AP) of the complement system. Here, we have identified Lufaxin, a protein component in saliva, as the inhibitor of the AP. Lufaxin inhibited the deposition of C3b, Bb, Properdin, C5b and C9b on agarose-coated plates in a dose dependent manner. It also inhibited the activation of factor B in normal serum, but had no effect on the components of the membrane attack complex. Surface plasmon resonance (SPR) experiments demonstrated that Lufaxin stabilizes the C3b-B proconvertase complex when passed over a C3b surface in combination with factor B. Lufaxin was also shown to inhibit the activation of factor B by factor D in a reconstituted C3b-B, but did not inhibit the activation of C3 by reconstituted C3b-Bb. Proconvertase stabilization does not require the presence of divalent cations, but addition of Ni2+ increases the stability of complexes formed on SPR surfaces. Stabilization of the C3b-B complex to prevent C3 convertase formation (C3b-Bb formation) is a novel mechanism that differs from previously described strategies used by other organisms to inhibit the AP of the host complement system.
  • Neutrophil extracellular traps reprogram IL-4/GM-CSF-induced monocyte differentiation to anti-inflammatory macrophages
    Anderson B. Guimarães-Costa, Natalia C. Rochael, Fabiano Oliveira, Juliana Echevarria-Lima, Elvira M. Saraiva
    Frontiers in Immunology, 2017
  • Neutrophil extracellular traps release induced by Leishmania: Role of PI3Kγ, ERK, PI3Kσ, PKC, and [Ca2+]
    Thiago DeSouza-Vieira, Anderson Guimarães-Costa, Natalia C Rochael, Maria N Lira, Michelle T Nascimento, Phillipe de Souza Lima-Gomez, Rafael M Mariante, Pedro M Persechini, Elvira M Saraiva
    Journal of Leukocyte Biology, 2016
  • Molecular Diversity between Salivary Proteins from New World and Old World Sand Flies with Emphasis on Bichromomyia olmeca, the Sand Fly Vector of Leishmania mexicana in Mesoamerica
    Maha Abdeladhim, Iliano V. Coutinho-Abreu, Shannon Townsend, Silvia Pasos-Pinto, Laura Sanchez, Manoochehr Rasouli, Anderson B. Guimaraes-Costa, Hamide Aslan, Ivo M. B. Francischetti, Fabiano Oliveira, Ingeborg Becker, Shaden Kamhawi, Jose M. C. Ribeiro, Ryan C. Jochim, Jesus G. Valenzuela
    Plos Neglected Tropical Diseases, 2016
  • Classical ROS-dependent and early/rapid ROS-independent release of Neutrophil Extracellular Traps triggered by Leishmania parasites
    Natalia C. Rochael, Anderson B. Guimarães-Costa, Michelle T. C. Nascimento, Thiago S. DeSouza-Vieira, Matheus P. Oliveira, Luiz F. Garcia e Souza, Marcus F. Oliveira, Elvira M. Saraiva
    Scientific Reports, 2015
  • A metabolic shift toward pentose phosphate pathway is necessary for amyloid fibril- and phorbol 12-myristate 13-Acetate-induced neutrophil extracellular trap (NET) formation
    Estefania P. Azevedo, Natalia C. Rochael, Anderson B. Guimarães-Costa, Thiago S. de Souza-Vieira, Juliana Ganilho, Elvira M. Saraiva, Fernando L. Palhano, Debora Foguel
    Journal of Biological Chemistry, 2015
  • Impact of insect salivary proteins in blood feeding, host immunity, disease, and in the development of biomarkers for vector exposure
    Iliano V Coutinho-Abreu, Anderson B Guimarães-Costa, Jesus G Valenzuela
    Current Opinion in Insect Science, 2015
  • A sand fly salivary protein vaccine shows efficacy against vector-transmitted cutaneous leishmaniasis in nonhuman primates
    Fabiano Oliveira, Edgar Rowton, Hamide Aslan, Regis Gomes, Philip A. Castrovinci, Patricia H. Alvarenga, Maha Abdeladhim, Clarissa Teixeira, Claudio Meneses, Lindsey T. Kleeman, Anderson B. Guimarães-Costa, Tobin E. Rowland, Dana Gilmore, Seydou Doumbia, Steven G. Reed, Phillip G. Lawyer, John F. Andersen, Shaden Kamhawi, Jesus G. Valenzuela
    Science Translational Medicine, 2015
  • 3'-nucleotidase/nuclease activity allows Leishmania parasites to escape killing by neutrophil extracellular traps
    Anderson B. Guimarães-Costa, Thiago S. DeSouza-Vieira, Rafael Paletta-Silva, Anita Leocádio Freitas-Mesquita, José Roberto Meyer-Fernandes, Elvira M. Saraiva
    Infection and Immunity, 2014
  • Warifteine, an alkaloid purified from cissampelos sympodialis, inhibits neutrophil migration in vitro and in vivo
    Thaline F. A. Lima, Juliana D. B. Rocha, Anderson B. Guimarães-Costa, José M. Barbosa-Filho, Débora Decoté-Ricardo, Elvira M. Saraiva, Luciana B. Arruda, Marcia R. Piuvezam, Ligia M. T. Peçanha
    Journal of Immunology Research, 2014
  • Amyloid fibrils trigger the release of neutrophil extracellular traps (NETs), causing fibril fragmentation by NET-associated elastase
    Estefania P.C. Azevedo, Anderson B. Guimarães-Costa, Guilherme S. Torezani, Carolina A. Braga, Fernando L. Palhano, Jeffery W. Kelly, Elvira M. Saraiva, Debora Foguel
    Journal of Biological Chemistry, 2012
  • ETosis: A microbicidal mechanism beyond cell death
    Anderson B. Guimarães-Costa, Michelle T. C. Nascimento, Amanda B. Wardini, Lucia H. Pinto-da-Silva, Elvira M. Saraiva
    Journal of Parasitology Research, 2012
  • Characterization of neutrophil extracellular traps in cats naturally infected with feline leukemia virus
    A. B. Wardini, A. B. Guimaraes-Costa, M. T. C. Nascimento, N. R. Nadaes, M. G. M. Danelli, C. Mazur, C. F. Benjamim, E. M. Saraiva, L. H. Pinto-da-Silva
    Journal of General Virology, 2010
  • Leishmania amazonensis promastigotes induce and are killed by neutrophil extracellular traps
    Anderson B. Guimarães-Costa, Michelle T. C. Nascimento, Giselle S. Froment, Rodrigo P. P. Soares, Fernanda N. Morgado, Fátima Conceição-Silva, Elvira M. Saraiva
    Proceedings of the National Academy of Sciences of the United States of America, 2009