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Id: lil-774286
Autor: Roberto Neto, João.
Título: Participação da Fosfatidilserina exposta por Toxoplasma gondii na indução de Corpúsculos Lipídicos em Macrófago / Phosphatidylserine participation exposed by Toxoplasma gondii in inducing corpuscles Lipid in Macrophage.
Fonte: Rio de Janeiro; s.n; 2013. viii,73 p. ilus, tab, graf.
Idioma: pt.
Tese: Apresentada a Instituto Oswaldo Cruz para obtenção do grau de Mestre.
Resumo: Toxoplasma gondii é o agente causador da toxoplasmose, doença distribuída em grande parte do globo infectando vertebrados endotérmicos. T. gondii é um parasita intracelular obrigatório e não sintetiza colesterol, recrutando-o da célula hospedeira.Esse parasito é dividido em grupos, de acordo com a virulência, sendo a cepa RH e a cepa ME-49 representantes de parasitos de maior e de moderada virulência,respectivamente. Semelhante a outros parasitos protozoários, T. gondii expõem fosfatidilserina (PS) na membrana externa, sendo um exemplo do mimetismo apoptótico, o que tem sido sugerido como mecanismo de evasão. Corpúsculos lipídicos (CL) são organelas lipídicas comumente encontradas em uma gama de diferentes células, de plantas, parasitos e animais. CL são modulados positiva mente por diferentes fatores, incluindo células apoptóticas, parasitos como Trypanosoma cruzi, Leishmania spp. e Plasmodium falciparum e citocinas, como o fator de transformação do crescimento (TGF-beta). Nosso trabalho visou investigar se a PSexposta na membrana plasmática de T. gondii pode induzir CL em macrófagos.Independente da virulência da cepa utilizada, T gondii foi capaz de induzir CL em macrófagos infectados. A indução foi maior com aumento da relação parasito/macrófago. Subpopulações de T. gondii, PS positivos (PS+) e PS negativo(PS-) foram obtidas e a subpopulação de PS + induziu mais CL em relação a subpopulação de PS-. A neutralização da PS dos parasitos PS+ ou da população total com anexina-V foi capaz de reduzir o número de CL nas células hospedeiras.Lipossomos contendo PS induziram mais CL em macrófagos quando comparados aos lipossomos sem PS. Curiosamente, parasitos PS- também foram capazes de aumentar o número de CL em macrófagos, sugerindo a participação de outros fatores nesse processo indutor. Após a interação de macrófagos com T. gondii,observamos aumento no número de CL tanto em células que continham o parasita quanto em células vizinhas não parasitadas...

Toxoplasma gondii is the causative agent of toxoplasmosis, a disease largely spreadacross the globe infecting almost any endothermic vertebrates. T. gondii is anobligatory intracellular parasite that can not synthesize cholesterol thus relying onrecruiting it from the host cell. This parasite is divided into groups according to thevirulence, and the RH strain and the ME-49 strain representing highly and moderatevirulent parasites, respectively. Similar to other protozoan parasites, T. gondiiexposes phosphatidylserine (PS) on the outer membrane, an example of theapoptotic mimicry, which has been suggested as a mechanism of evasion,. Lipidbodies (LB) are lipid organelles commonly found in a range of different cells of plants,animals and parasites. LB are positively modulated by different factors, includingapoptotic cells, parasites such as Trypanosoma cruzi, Leishmania spp. andPlasmodium falciparum and cytokines such as transforming growth factor (TGF-beta) .Our study aimed to investigate whether the PS exposed on the plasma membrane ofT. gondii in macrophages can induce LB. T gondii was capable of inducing LB ininfected macrophages, independently of the virulence of the strain used. The LBinduction was greater with increase in parasite / macrophage ratio. Subpopulations ofT gondii positive PS (PS+) and negative (PS-) were obtained and PS+ subpopulationinduced significantly greater LB formation compared to PS- subpopulation. Theneutralization of PS with annexin - V was able to reduce the number of LB on PS+parasites or on the total parasite population, but not on PS- parasites. Liposomescontaining PS induced more LB than liposomes without PS...
Descritores: Células Sanguíneas
Macrófagos
Fosfatidilserinas
Toxoplasma/imunologia
-Apoptose
Responsável: BR15.1 - Biblioteca de Ciências Biomédicas


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Texto completo SciELO Brasil
Texto completo
Id: lil-685490
Autor: Memorias do Instituto Oswaldo Cruz; Rochael, Natalia Cadaxo; Lima, Luize Goncalves; Oliveira, Sandra Maria Pereira de; Barcinski, Marcello Andre; Saraiva, Elvira Maria; Monteiro, Robson Queiroz; Pinto-da-Silva, Lucia Helena.
Título: Leishmania amazonensis exhibits phosphatidylserine-dependent procoagulant activity, a process that is counteracted by sandfly saliva
Fonte: Mem. Inst. Oswaldo Cruz;108(6):679-685, set. 2013. graf.
Idioma: en.
Resumo: Leishmania parasites expose phosphatidylserine (PS) on their surface, a process that has been associated with regulation of host's immune responses. In this study we demonstrate that PS exposure by metacyclic promastigotes of Leishmania amazonensis favours blood coagulation. L. amazonensis accelerates in vitro coagulation of human plasma. In addition, L. amazonensis supports the assembly of the prothrombinase complex, thus promoting thrombin formation. This process was reversed by annexin V which blocks PS binding sites. During blood meal, Lutzomyia longipalpis sandfly inject saliva in the bite site, which has a series of pharmacologically active compounds that inhibit blood coagulation. Since saliva and parasites are co-injected in the host during natural transmission, we evaluated the anticoagulant properties of sandfly saliva in counteracting the procoagulant activity of L. amazonensis . Lu. longipalpis saliva reverses plasma clotting promoted by promastigotes. It also inhibits thrombin formation by the prothrombinase complex assembled either in phosphatidylcholine (PC)/PS vesicles or in L. amazonensis . Sandfly saliva inhibits factor X activation by the intrinsic tenase complex assembled on PC/PS vesicles and blocks factor Xa catalytic activity. Altogether our results show that metacyclic promastigotes of L. amazonensis are procoagulant due to PS exposure. Notably, this effect is efficiently counteracted by sandfly saliva.
Descritores: Coagulação Sanguínea/fisiologia
Leishmania/metabolismo
Fosfatidilserinas/metabolismo
Psychodidae/parasitologia
Saliva/metabolismo
-Anticoagulantes/metabolismo
Cisteína Endopeptidases
Fator V/antagonistas & inibidores
Fator X/antagonistas & inibidores
Fator Xa/antagonistas & inibidores
Insetos Vetores/parasitologia
Proteínas de Neoplasias/antagonistas & inibidores
Tempo de Tromboplastina Parcial
Fosfatidilcolinas/metabolismo
Psychodidae/metabolismo
Trombina/antagonistas & inibidores
Extratos de Tecidos/metabolismo
Limites: Animais
Humanos
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: BR1.1 - BIREME


  3 / 14 LILACS  
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Id: lil-595037
Autor: López-Herrera, A; Ruiz-Sáenz, J; Góez, Y. P; Zapata, W; Velilla, P. A; Arango, A. E; Urcuqui-Inchima, S.
Título: Apoptosis as pathogenic mechanism of infection with vesicular stomatitis virus: evidence in primary bovine fibroblast cultures
Fonte: Biocell;33(2):121-132, Aug. 2009. graf.
Idioma: en.
Resumo: To determine whether fibroblasts from Blanco Orejinegro cattle, exhibit any level of resistance to infection against vesicular stomatitis virus (VSV) serotypes Indiana (VSV-I) or New Jersey (VSV-NJ), 30 fibroblast cultures were phenotyped to evaluate their resistance/susceptibility. Thirty three % of Blanco Orejinegro fibroblast cultures were classified as very resistant, 50% as resistant, and 17% as susceptible to VSV-I infection, whereas 20% were classified as very resistant, 50% as resistant and 30% as susceptible to VSV-NJ infection. Therefore, there appears to be a large variation in phenotypic polymorphism among the fibroblasts to infection by VSV. To elucidate the mechanisms responsible for this diversity, we searched for a possible relationship between resistance/ susceptibility and production of factors wi th antiviral activity; however fibroblasts did not secrete factors with antiviral activity. We examined also whether apoptosis where induced by infection and its correlation with the polymorphism of resistance/susceptibility to VSV. Using morphological analyses, hypoploidy measurements, and level of phosphatidyl serine expression, high levels of apoptosis were measured in VSV infected fibroblasts. However, no correlation exists between apoptosis and the category of resistance/susceptibility to infection, indicating that apoptosis is a pathogenic mechanism of VSV.
Descritores: Antivirais/metabolismo
Fibroblastos/patologia
Fibroblastos/virologia
Fosfatidilserinas/metabolismo
Frações Subcelulares/metabolismo
Infecções por Rhabdoviridae/patologia
Infecções por Rhabdoviridae/virologia
Membrana Celular/metabolismo
-Apoptose
Forma Celular
Células Cultivadas
Fenótipo
Ploidias
Limites: Bovinos
Animais
Responsável: AR40.1 - Biblioteca de la Facultad de Ciencias Médicas de la UNCuyo


  4 / 14 LILACS  
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Texto completo SciELO Brasil
Texto completo
Id: lil-538168
Autor: Torrentes-Carvalho, Amanda; Azeredo, Elzinandes L; Reis, Sonia RI; Miranda, Alessandro S; Gandini, Mariana; Barbosa, Luciana S; Kubelka, Claire F.
Título: Dengue-2 infection and the induction of apoptosis in human primary monocytes
Fonte: Mem. Inst. Oswaldo Cruz;104(8):1091-1099, Dec. 2009. ilus.
Idioma: en.
Resumo: Monocytes/macrophages are important targets for dengue virus (DENV) replication; they induce inflammatory mediators and are sources of viral dissemination in the initial phase of the disease. Apoptosis is an active process of cellular destruction genetically regulated, in which a complex enzymatic pathway is activated and may be trigged by many viral infections. Since the mechanisms of apoptotic induction in DENV-infected target cells are not yet defined, we investigated the virus-cell interaction using a model of primary human monocyte infection with DENV-2 with the aim of identifying apoptotic markers. Cultures analyzed by flow cytometry and confocal microscopy yielded DENV antigen positive cells with rates that peaked at the second day post infection (p.i.), decayed afterwards and produced the apoptosis-related cytokines TNF-á and IL-10. Phosphatidylserine, an early marker for apoptosis, was increased at the cell surface and the Fas death receptor was upregulated at the second day p.i. at significantly higher rates in DENV infected cell cultures than controls. However, no detectable changes were observed in the expression of the anti-apoptotic protein Bcl-2 in infected cultures. Our data support virus modulation of extrinsic apoptotic factors in the in vitro model of human monocyte DENV-2 infection. DENV may be interfering in activation and death mechanisms by inducing apoptosis in target cells.
Descritores: Apoptose/imunologia
Vírus da Dengue/fisiologia
Dengue/virologia
Monócitos/patologia
-/imunologia
ANTIGENS, CDACETIC ANHYDRIDES/imunologia
Vírus da Dengue/classificação
Vírus da Dengue/imunologia
Dengue/imunologia
Citometria de Fluxo
/imunologia
INTERLEUKIN-ABDUCENS NERVE/imunologia
Microscopia Confocal
Monócitos/imunologia
Monócitos/virologia
Fosfatidilserinas/imunologia
Fatores de Tempo
Fator de Necrose Tumoral alfa/imunologia
Limites: Humanos
Responsável: BR1.1 - BIREME


  5 / 14 LILACS  
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Urbanetz, Almir Antonio
Carvalho, Newton Sérgio de
Id: lil-534076
Autor: Schuffner, Alessandro; Urbanetz, Almir Antonio; Carvalho, Newton Sergio de; Oliveira, Maria Theresa Costa Ramos de; Drechmer, Mariana; Placido, Thiago.
Título: Morte celular programada e peroxidação lipídica no espermatozoide humano / Programed cell death and lipid peroxidation in human spermatozoa
Fonte: Femina;37(6):313-318, jun. 2009. ilus.
Idioma: pt.
Resumo: O principal marcador bioquímico da apoptose precoce em células somáticas é a translocação da fosfatidilserina para o folheto externo da membrana plasmática e fragmentação do DNA. Essas características têm sido também descritas em espermatozoides e são observadas com maior frequência nos ejaculados de homens inférteis. O espermatozoide humano tem uma alta concentração de ácidos graxos poliinsaturados em sua membrama e pouca proteção adequada com antioxidante. Ácidos graxos poli-insaturados são necessários para eventos de fusão da membrana associados à fertilização. No entanto, a presença deles acarreta uma vulnerabilidade para os danos peroxidativos. Sob várias condições de tensão oxidativa, o início da cascata da peroxidação lipídica resulta em perda da fluidez e prejuízo da função espermática. No campo da reprodução humana, principalmente nos aspectos referentes à infertilidade masculina, conhecer os mecanismos da apoptose e da peroxidação lipídica é essencial. Na abordagem da infertilidade masculina, a avaliação da translocação da fosfatidilserina (através da aderência à anexia V como marcador da apoptose) e a aferição da peroxidação lipídica têm como objetivo tentar identificar os casos com mau prognóstico na criopreservação/descongelamento. A identificação de tais casos poderia evitar desgastes psicológicos e econômicos nesses pacientes, bem como a indicação de uma outra abordagem para o seu acompanhamento.

Plasma membrane translocation of phosphatidylserine and DNA fragmentation are considered the main biochemical markers of early apoptosis in somatic cells. These characteristics have been also described in sperm cells and are commonly observed in ejaculated infertile men. The membrane of human spermatozoa contains a high concentration of polyunsaturated fatty acids and inadequate antioxidative protection. Although polyunsaturated fatty acids are required in membrane events associated with potential fertilization, their appearance may increase the vulnerability to peroxidative damage. Under oxidative stress, lipid peroxidation results in motility and sperm function damage. In the field of human reproduction, mainly in the area of male infertility, it is essential to know the apoptosis mechanism and the effects of lipid peroxidation. In the study of male infertility, the evaluation of plasma membrane phosphatidylserine translocation (assessed by annexin V binding as a apoptosis marker) and spontaneous lipid peroxidation aim to identify the bad prognostic cases for those that are submitted to cryopreservation process stress. This would prevent psychological and economic losses in these patients and establish another evaluation method for their infertility.
Descritores: Apoptose
Transporte Biológico
Morte Celular
Criopreservação
Espermatozoides/fisiologia
Espermatozoides/metabolismo
Fosfatidilserinas/metabolismo
Peroxidação de Lipídeos
-Infertilidade Masculina
Limites: Masculino
Responsável: BR1365.1 - Biblioteca Biomédica A - CB/A


  6 / 14 LILACS  
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Id: lil-500657
Autor: Deolindo, Poliana.
Título: Exposição de fosfatidilserina em amastigotas intracelulares de Leishmania (L) amazonensis e seu papel na modulação da resposta macrofágica / Exposition of phosphatidylserine in amastigotes intracellular of Leishmania (L) amazonensis and its paper in the modulation of the macrophage reply.
Fonte: Rio de Janeiro; s.n; 2008. viii,128 p. ilus, tab, graf.
Idioma: pt.
Tese: Apresentada a Instituto Oswaldo Cruz para obtenção do grau de Doutor.
Resumo: Os macrófagos são as células preferenciais para a infecção e a proliferação de parasitas do gênero Leishmania. A sobrevivência do parasita e o desenvolvimento da infecção são resultado direto da evasão do parasita dos mecanismos microbicidas do hospedeiro. As formas amastigotas de Leishmania (L) amazonensis isoladas de lesãoes em camundongos espõem o fosfolipídio fosfatidilserina (PS) na face externa da sua membrana plasmática, um fenômeno descrito como Mimetismo Apoptótico. O reconhecimento deste fosfolipídio pelo macrófago induz a internalização do parasita por um mecanismo de macropinocitose, a produção de citocinas anti-inflamatórias IL-10 e TGF-Beta e inibe a produção de óxido nítrico (NO), contribuindo para o aumento da infectividade do parasita e sua proliferação na célula hospedeira. A exposição de PS na superfície das amastigotas pode ser modulada pelo hospedeiro: amastigotas isoladas de lesões em camundongos BALB/c expõem mais moléculas de PS na superfície que aquelas isoladas de camundongos C57BL/6. Neste trabalho demonstramos que amastigotas purificadas de macrófagos de camundongos BALB/c e C57BL/6 infectados in vitro não apresentam diferenças significativas na exposição de PS na superfície, sugerindo que as diferenças observadas no modelo in vivo são dependentes de uma ativação diferencial dos macrófagos no hospedeiro. Amastigotas isoladas de lesão em camundongos BALB/c(nu/nu) expõem menos PS na superfície que aquelas isoladas de lesões em camundongos BALB/c, indicando um papel das citocinas produzidas pelas células T na modulação da exposição de PS pelo parasita. Durante o processo de diferenciação de promastigota para amastigota no interior do vacúolo parasitóforo ocorre aumento na exposição de PS na superfície externa da membrana do parasita. Neste período, observamos indução de macropinocitose nos macrófagos infectados e fusão das vesículas macropinocíticas com o vacúolo contendo os parasitas, sugerindo que a exposição de PS pela...infecção.
Descritores: Apoptose
Leishmania
Ativação de Macrófagos
Fosfatidilserinas
Limites: Animais
Camundongos
Responsável: BR15.1 - Biblioteca de Ciências Biomédicas
BR15.1


  7 / 14 LILACS  
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Texto completo SciELO Brasil
Texto completo
Id: lil-492886
Autor: Hu, T; Shi, J; Jiao, X; Zhou, J; Yin, X.
Título: Measurement of annexin V uptake and lactadherin labeling for the quantification of apoptosis in adherent Tca8113 and ACC-2 cells
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;41(9):750-757, Sept. 2008. graf, tab.
Idioma: en.
Projeto: Province Science Foundation of Heilongjiang Science and Technology Bureau.
Resumo: Phosphatidylserine (PS) exposure occurs during the cell death program and fluorescein-labeled lactadherin permits the detection of PS exposure earlier than annexin V in suspended cell lines. Adherent cell lines were studied for this apoptosis-associated phenomenon to determine if PS probing methods are reliable because specific membrane damage may occur during harvesting. Apoptosis was induced in the human tongue squamous carcinoma cell line (Tca8113) and the adenoid cystic carcinoma cell line (ACC-2) by arsenic trioxide. Cells were harvested with a modified procedure and labeled with lactadherin and/or annexin V. PS exposure was localized by confocal microscopy and apoptosis was quantified by flow cytometry. The detachment procedure without trypsinization did not induce cell damage. In competition binding experiments, phospholipid vesicles competed for more than 95 and 90 percent of lactadherin but only about 75 and 70 percent of annexin V binding to Tca8113 and ACC-2 cells. These data indicate that PS exposure occurs in three stages during the cell death program and that fluorescein-labeled lactadherin permitted the detection of early PS exposure. A similar pattern of PS exposure has been observed in two malignant cell lines with different adherence, suggesting that this pattern of PS exposure is common in adherent cells. Both lactadherin and annexin V could be used in adherent Tca8113 and ACC-2 cell lines when an appropriate harvesting procedure was used. Lactadherin is more sensitive than annexin V for the detection of PS exposure as the physical structure of PS in these blebs and condensed apoptotic cell surface may be more conducive to binding lactadherin than annexin V.
Descritores: Apoptose
/metabolismo
ANNEXIN AABDOMEN/metabolismo
Antígenos de Superfície/metabolismo
Proteínas do Leite/metabolismo
Fosfatidilserinas/metabolismo
-Adesão Celular
Linhagem Celular Tumoral
Carcinoma Adenoide Cístico/metabolismo
Carcinoma Adenoide Cístico/patologia
Carcinoma de Células Escamosas/metabolismo
Carcinoma de Células Escamosas/patologia
Citometria de Fluxo
Fluoresceína
Corantes Fluorescentes
Microscopia Confocal
Neoplasias da Língua/metabolismo
Neoplasias da Língua/patologia
Limites: Animais
Bovinos
Humanos
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: BR1.1 - BIREME


  8 / 14 LILACS  
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Souza, Wanderley de
Texto completo
Id: lil-467600
Autor: Rodrigues, Juliany Cola Fernandes; Seabra, Sérgio Henrique; Souza, Wanderley de.
Título: Apoptosis-like death in parasitic protozoa
Fonte: Braz. j. morphol. sci = Rev. bras. ciênc. morfol;23(1):87-98, jan.-mar. 2006. ilus, tab.
Idioma: en.
Resumo: Apoptosis is an essential physiological process that plays a critical role in development and tissue homeostasis in multicellular organisms, but which is also observed in several eukaryotic microorganisms such as yeast and protozoa. Here, the authors briefly review the most used techniques to detect apoptosis in mammalian cells, especially those that can be applied to parasitic protozoa after different conditions such as drugtreatment. Apoptosis-like processes have been described in protozoa which present mitochondria, such as members of the Kinetoplastida and Apicomplexa groups as well as in protozoa which do not have a mitochondrion, as Entamoeba, Trichomonas and Giardia do. These observations are of interest from an evolutive point of view, especially due to the fact that the participation of the mitochondria in apoptosis has been extensively analyzed in several biological systems. The authors also reviewed the available data showing that several drugs in use as anti-protozoa agents, as well as others which are in the development phase, kill the protozoa through an apoptotic-like process.
Descritores: Apoptose
Apoptose
Leishmania
Leishmania/citologia
Necrose
Fosfatidilserinas
Trypanosoma
-Apoptose/fisiologia
Morte Celular
Tratamento Farmacológico
Fosfatidilserinas/biossíntese
Tipo de Publ: Revisão
Responsável: BR734.1 - Biblioteca Central Cesar Lattes - BCCL


  9 / 14 LILACS  
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Texto completo SciELO Chile
Texto completo
Id: lil-443668
Autor: Zago, M. P; Verstraeten, S. V; Oteiza, P. I.
Título: Zinc in the prevention of Fe2+-initiated lipid and protein oxidation
Fonte: Biol. Res;33(2):143-150, 2000. graf.
Idioma: en.
Projeto: University of Buenos Aires, Argentina.
Resumo: In the present study we characterized the capacity of zinc to protect lipids and proteins from Fe2+-initiated oxidative damage. The effects of zinc on lipid oxidation were investigated in liposomes composed of brain phosphatidylcholine (PC) and phosphatidylserine (PS) at a molar relationship of 60:40 (PC:PS, 60:40). Lipid oxidation was evaluated as the oxidation of cis-parinaric acid or as the formation of 2-thiobarbituric acid-reactive substances (TBARS). Zinc protected liposomes from Fe2+ (2.5-50 microM)-supported lipid oxidation. However, zinc (50 microM) did not prevent the oxidative inactivation of glutamine synthetase and glucose 6-phosphate dehydrogenase when rat brain supernatants were oxidized in the presence of 5 microM Fe2+ and 0.5 mM H2O2. We also studied the interactions of zinc with epicatechin in the prevention of lipid oxidation in liposomes. The simultaneous addition of 0.5 microM epicatechin (EC) and 50 microM zinc increased the protection of liposomes from oxidation compared to that observed in the presence of zinc or EC separately. Zinc (50 microM) also protected liposomes from the stimulatory effect of aluminum on Fe2+-initiated lipid oxidation. Zinc could play an important role as an antioxidant in biological systems, replacing iron and other metals with pro-oxidant activity from binding sites and interacting with other components of the oxidant defense system.
Descritores: Antioxidantes/farmacologia
Catequina/farmacologia
Compostos Ferrosos/farmacologia
Peroxidação de Lipídeos/efeitos dos fármacos
Zinco/farmacologia
-Interações Medicamentosas
Fosfatidilcolinas/metabolismo
Fosfatidilserinas/metabolismo
Lipídeos de Membrana/metabolismo
Lipossomos/metabolismo
Ratos Wistar
Substâncias Reativas com Ácido Tiobarbitúrico
Limites: Ratos
Animais
Responsável: BR1.1 - BIREME


  10 / 14 LILACS  
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Texto completo SciELO Brasil
Texto completo
Id: lil-402670
Autor: Wanderley, J. L. M; Benjamin, A; Real, F; Bonomo, A; Moreira, M. E. C; Barcinski, M. A.
Título: Apoptotic mimicry: an altruistic behavior in host/Leishmania interplay
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;38(6):807-812, June 2005. ilus.
Idioma: en.
Conferência: Apresentado em: Congresso Brasileiro de Biologia Celular, 11, Campinas, July 15-18, 2004.
Resumo: Apoptosis is the most common phenotype observed when cells die through programmed cell death. The morphologic and biochemical changes that characterize apoptotic cells depend on the activation of a diverse set of genes. Apoptosis is essential for multicellular organisms since their development and homeostasis are dependent on extensive cell renewal. In fact, there is strong evidence for the correlation between the emergence of multicellular organisms and apoptosis during evolution. On the other hand, no obvious advantages can be envisaged for unicellular organisms to carry the complex machinery required for programmed cell death. However, accumulating evidence shows that free-living and parasitic protozoa as well as yeasts display apoptotic markers. This phenomenon has been related to altruistic behavior, when a subpopulation of protozoa or yeasts dies by apoptosis, with clear benefits for the entire population. Recently, phosphatidylserine (PS) exposure and its recognition by a specific receptor (PSR) were implicated in the infectivity of amastigote forms of Leishmania, an obligatory vertebrate intramacrophagic parasite, showing for the first time that unicellular organisms use apoptotic features for the establishment and/or maintenance of infection. Here we focus on PS exposure in the outer leaflet of the plasma membrane - an early hallmark of apoptosis - and how it modulates the inflammatory activity of phagocytic cells. We also discuss the possible mechanisms by which PS exposure can define Leishmania survival inside host cells and the evolutionary implications of apoptosis at the unicellular level.
Descritores: Apoptose/fisiologia
Leishmania/fisiologia
Fosfatidilserinas/fisiologia
-Apoptose/imunologia
Arginase/metabolismo
Interações Hospedeiro-Parasita/imunologia
Interações Hospedeiro-Parasita/fisiologia
Sistema Imunitário/fisiologia
Leishmania/imunologia
Macrófagos/fisiologia
Fosfatidilserinas/imunologia
Limites: Animais
Tipo de Publ: Revisão
Responsável: BR1.1 - BIREME



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