Browsing by Autor "Antonio Moreno Hernández"

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Atomic Force Microscopy of host cell-amastigote interaction in cutaneous leishmaniasis
(2004) Ana Lugo de Yarbuh; Cesare Colasante; Marcos Eduardo Valdés Alarcón; Antonio Moreno Hernández
Abstract: Natural infection produced by the entry of promastigotes into the skin cells induces cutaneous leishmaniasis disease and the Interaction between phagocytic cells and different strains of Leishmania determine the course of disease in the mammalian host. In this study the cutaneous lesions from hamsters infected with the L. garnhami were pressed on a microscope slide, allowed to dry and methanol-fixed in order to be ultrastructurally analyzed using atomic force microscopy (AFM). Free amastigotes showed their nucleus, kinetoplast and a depression of 5 microns, corresponding to the refractil organelle characteristic of this Leishmania. Parasites inside macrophages and lymphocytes and the topographical relationship with the host cytoplasm was also observed. Parasite-host-cell interaction revealed different membrane contact. The amastigote-macrophage contact is established by small macrophage filopodio associated with its cytoplasmic reduction near the contact site of 800 nm. The amastigote-lymphocyte contact shows fusion-like behavior between the two membranes without any cell specialization. The cutaneous lesion studied with AFM allowed observation with high resolution the close contact established between the parasite and its host cells as well as details of the fine structure of the amastigotes, applying a simple and rapid tissue preparation. Resumen: La infección natural producida por la entrada de promastigotes en la piel produce leishmaniasis cutánea y la interacción entre las células fagocíticas y las diferentes cepas de Leishmania determina el curso de la enfermedad en el hospedador vertebrado. En este estudio las lesiones cutáneas de hamsteres infectados con L. garnhami fueron frotadas sobre un portaobjeto, secadas a temperatura ambiente y fijadas con metanol para analizarlas ultraestructuralmente usando un microscopio de fuerza atómica (AFM). Los amastigotes mostraron el núcleo, kinetoplasto y una depresión de 5µ, correspondiente a la organela refráctil característica de esta especie. Los parásitos dentro de los macrófagos y de linfocitos y las relaciones topográficas con el citoplasma de la célula hospedadora, revelaron diferentes tipos de contacto entre las membranas celulares. El contacto amastigote-macrófago se establece por un pequeño filopodio del macrófago asociado con reducción citoplasmática cerca del sitio de contacto de 800 nm. El conctato amastigote-linfocito mostró estrecha fusión entre las dos membranas sin ninguna especialización celular. Concluimos que las lesiones cutánes estudiadas con AFM permite la observación con alta resolución, del estrecho contacto que se establece entre los parasites y sus células hospedadoras así como, los detalles de la ultraestructura de los amastigotes aplicando una simple y rápida preparación de las muestras de tejido.
Digestive Tract Dilatation of Mice Infected with Trypanosoma Cruzi
(2001) Brizeida Guillén-Pernía; Ana Lugo-Yarbuh; Antonio Moreno Hernández
The Effects of Ingesting a High-fat Diet on Wistar Rats Chronically Infected with Trypanosoma cruzi
(2009) José Leonardo Paredes; Antonio Moreno Hernández; Gloria Premoli; Maritza Alarcón; Ana Lugo de Yarbuh; J Moreno Villarreal; Sónia Araújo; Rafael J. Borges
The effects of ingesting a high fat diet on albino rats (R. norvegicus) chronically infected with Trypanosome cruzi “Planalto” were researched using serological and parasitological diagnostic tests, body mass index (BMI) quantification, detection of C-Protein Reactive (CPR), evaluation of the plasmatic lipid levels (total cholesterol, high density lipoproteins HDL and triglycerides) and the presence of lipidic deposits in the aorta artery. During the course of the chagasic infection, patent parasitemias were detected between the ages of 10 and 35 days post-infection (pi) with a maximum average of 36.68 ± 2 tryps/mm³ of blood at 25 days. At 90 days pi, the absence of parasitemias and the presence of IgG anti T. cruzi antibodies were in evidence. The chagasic rats in chronic phase (A) and the healthy controls (C) submitted to a high fat diet showed: 1. Significant variations (p0.05) in the BMI, in comparison with the rat groups receiving a normal diet (B: infected and D: healthy rats); 2. A discrete CRP reaction in the serum of infected rats B; 3. A significant increase was shown in the total cholesterol levels, HDL cholesterol and triglycerides for groups A and C in comparison with control groups B and D (p0.05). The histological study of rat arteries in group A revealed important lipid deposits located in the muscular layer near the intimal and adventitial layer. These results suggest that the increase in plasmatic lipid levels stimulated by the infectious process are the main mechanisms through which T. cruzi could be influencing the initiation or the progression of atheromatous plaque.
The Resistance of Chagasic Wistar Rat Offspring to Reinfections by Trypanosoma cruzi
(2012) Nora Mogollón; Antonio Moreno Hernández; Maritza Alarcón; Ana Lugo de Yarbuh; Martha Gloribet Ceballos Ramírez; Rafael Borges
The resistance to reinfection by Trypanosome cruzi in chagasic rat offspring was evaluated. Thirty male offspring () from infected mothers and 30 offspring from healthy mothers were used, divided into groups of 10 offspring each (I, II, III) and (IV, V, VI). The groups (I, IV) and (II, V) were inoculated and reinoculated by intradermal route with 5 × 104 metacyclic trypomastigotes of homologous (pL) and heterologous (Y) strains of T. cruzi, from laboratory infected Rhodnius prolixus, at one-month intervals. The control groups (III, VI) received saline injections. The parasitological and serological testing performed on both groups of infected offspring at 10, 20 and 30 days post-reinoculation (pr) showed significantly higher parasitemia levels in offspring from healthy mothers during the acute phase of the primary infection, the absence of bloodstream trypomastigotes after the 1st and 2nd reinoculation, and a significant increase in anti-T. cruzi antibody levels after initial inoculation and reinoculations. The histopathological and immunohistochemical analysis of heart and skeletal muscle sections from the offspring sacrificed at 45, 75 and 105 days pi, revealed the gradual establishment of myocarditis and acute myositis of variable intensity accompanied by few nests of amastigotes, a worsening of the pathologic picture produced by the initial inoculation, and the presence of abundant antigenic deposits that intensified with the reinoculations. In conclusion, the resistance of offspring born from chm to homologous and heterologous reinfection by T. cruzi strains, is produced, first, by vertical transmission of the parasites and/or humoral antibodies from infected mothers to their progeny, and second, by a sensibilization process in the host from continuous antigenic downloads produced when the inoculated parasites are destroyed.
[Trypanosoma cruzi infection in pregnant mice induces a cellular immune response with citokines production in their fetuses].
(National Institutes of Health, 2011) Maritza Alarcón; Loredana Goncalves; Cesare Colasante; Sonia Araujo; Antonio Moreno Hernández; Mary Carmen Pérez-Aguilar
The objective of this study was to detect the cytokines IFN-gamma, IL-4 and IL-10 expressed by CD4+ T cells in tissues of fetal mice with acute chagasic infection. For this, we examined the fetuses of NMRI mice whose mothers were infected with 22x10(3) metacyclic trypomastigotes of the M/HOM/BRA/53/Y strain of T. cruzi and made pregnant during the acute phase of infection. For the detection and localization of inflammatory infiltrates, nest parasites, antigens of T. cruzi a nd cytokines w eused hematoxylin-eosin techniques, peroxidase-anti-peroxidase and immunofluorescence. The immunohistochemical study revealed the presence of inflammatory infiltrates and antigens with amastigote nests in fetal skeletal muscle. CD4 + T cells producing IFN-gamma, as well as deposits of IFN-gamma and IL-10, were detected in sections of placenta, heart and skeletal muscle of fetuses of mice infected, while CD4+/IL-10+ was found only in skeletal muscle; in addition, deposits of IL-4 were detected only in placentas of healthy mice. These results indicate that fetuses are capable of generating their own immune response to antigens transmitted by their mother, which induces the secretion of cytokines and that, acting in synergy with the maternal antibodies, confer them a state of protection against infection; and that the transmission of the parasite depends on factors specific to each mother, which may modify its ability to control such transmission at the placental or systemic levels.