Encephalitozoon intestinalis:Humoral Responses in Interferon-γ Receptor Knockout Mice Infected with a Microsporidium Pathogenic in AIDS Patients

Fakhry, Youssef El; Achbarou, Abderrahim; Mazier, Dominique

doi:10.1006/expr.1998.4267

Cited by 42 publications

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“…Interestingly, immune sera from both control and IFN-␥R Ϫ mice recognized a series of E. intestinalis proteins. This differs from the findings of El Fakhry et al (13), which showed an increase in immunoglobulin G levels in IFN-␥R Ϫ mice but no increase in antibody levels in controls. In our study, by day 29 postinfection, serum antibody levels in IFN-␥R Ϫ mice were sufficient to detect several immunogenic proteins, including SWP1 and SWP2.…”

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confidence: 99%

“…) and wild-type mice (129S3/SvImJ) (Jackson Laboratory, Bar Harbor, Maine) were infected orally with 2 ϫ 10 8 E. intestinalis spores in H 2 O as previously described (13). Pooled infected or control sera were collected from each mouse on days 15, 29, 45, and 60 postinfection and used at 1:500 in Western blot analysis.…”

Section: Mouse Infection Model Gamma Interferon Receptor Null (Ifn-␥rmentioning

confidence: 99%

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Developmental Expression of Two Spore Wall Proteins during Maturation of the Microsporidian Encephalitozoon intestinalis

et al. 2001

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Microsporidia are intracellular eukaryotes that infect many animals and cause opportunistic infections in AIDS patients. The disease is transmitted via environmentally resistant spores. Two spore wall constituents from the microsporidian Encephalitozoon intestinalis were characterized. Spore wall protein 1 (SWP1), a 50-kDa glycoprotein recognized by monoclonal antibody (MAb) 11B2, was detected in developing sporonts and at low levels on the surfaces of mature spores. In contrast, SWP2, a 150-kDa glycoprotein recognized by MAb 7G7, was detected on fully formed sporonts and was more abundant on mature spores than SWP1. Nevertheless, the SWPs appeared to be complexed on the surfaces of mature spores. SWP1 and SWP2 are similar at the DNA and protein levels and have 10 conserved cysteines in the N-terminal domain, suggesting similar secondary structures. The C-terminal domain of SWP2 has a unique region containing 50 repeating 12-or 15-amino-acid units that lacks homology to known protein motifs. Antibodies from mice infected with E. intestinalis recognized SWP1 and SWP2. The characterization of two immunogenic SWPs from E. intestinalis will allow the study of exospore structure and function and may lead to the development of useful tools in the diagnosis and treatment of microsporidiosis.Microsporidia are obligate intracellular organisms that infect a wide variety of animals ranging from insects and fish to mammals, including humans. Of over 1,000 microsporidial species identified, at least 13 are known to infect humans (10). The species more commonly identified in humans are members of the families Enchephalitozoonidae and Enterocytozoonidae. In humans, microsporidiosis is found mostly in human immunodeficiency virus-infected and AIDS patients and commonly results in severe diarrhea and wasting (3,20). However, microsporidiosis also occurs in immunocompetent individuals and common farm animals (21,29,32).Microsporidia infect cells by a unique mechanism (reviewed in reference 31). Upon close association of a spore with a suitable host cell, a hollow polar filament is extruded from the spore into the host cell's cytoplasm. The infectious sporoplasm passes through the polar filament into the cell, initiating infection (18). Alternatively, the spore may be internalized by phagocytosis (33). The microsporidia then enter a stage of proliferative growth by nuclear fission called merogony, resulting in large and less structurally defined cells. In the family Encephalitozoonidae, the transition from meront to the next stage (sporont) is marked by aggregation of electron-dense material on the outer spore membrane. These immature cells are localized to the edge of the parasitophorous vacuole (PV). Then, in most cases, fully formed sporonts break away from the edge of the PV to reside internally (7, 12). Sporonts undergo continuous transition into sporoblasts, after which organelles organize and become more defined. At this stage, the cells form an electron-lucent material, the endospore, immediately inside the exospore region...

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Section: Mouse Infection Model Gamma Interferon Receptor Null (Ifn-␥rmentioning

confidence: 99%

Developmental Expression of Two Spore Wall Proteins during Maturation of the Microsporidian Encephalitozoon intestinalis

et al. 2001

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“…Intestinal and systemic E. intestinalis infections have been documented in several strains of immunosuppressed mice. 1,49,143 E. hellem administered intraperitoneally to athymic nude mice results in similar gross and histologic lesions as seen in E. cuniculi-infected immunoincompetent mice. 42 Spontaneous infections with E. intestinalis, E. hellem, or Enterocytozoon bieneusi have not been described in mice.…”

Section: Infection In Micementioning

confidence: 66%

Mammalian Microsporidiosis

2000

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Abstract. The phylum Microspora contains a diverse group of single-celled, obligate intracellular protozoa sharing a unique organelle, the polar filament, and parasitizing a wide variety of invertebrate and vertebrate animals, including insects, fish, birds, and mammals. Encephalitozoon cuniculi is the classic microsporidial parasite of mammals, and encephalitozoonosis in rabbits and rodents has been and continues to be recognized as a confounding variable in animal-based biomedical research. Although contemporary research colonies are screened for infection with this parasite, E. cuniculi remains a cause of morbidity and mortality in pet and conventionally raised rabbits. In addition, E. cuniculi is a potential pathogen of immature domestic dogs and farm-raised foxes. The recent discovery and identification of Encephalitozoon intestinalis, Encephalitozoon hellem, and Enterocytozoon bieneusi, in addition to E. cuniculi, as opportunistic pathogens of humans have renewed interest in the Microspora. Veterinary pathologists, trained in the comparative anatomy of multiple animal species and infectious disease processes, are in a unique position to contribute to the diagnosis and knowledge of the pathogenesis of these parasitic diseases. This review article covers the life cycle, ultrastructure, and biology of mammalian microsporaidia and the clinical disease and lesions seen in laboratory and domestic animals, particularly as they relate to Encephalitozoon species. Human microsporidial disease and animal models of human infection are also addressed. Often thought of as rabbit pathogens of historical importance, E. cuniculi and the related mammalian microsporidia are emerging as significant opportunistic pathogens of immunocompromised individuals.

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“…Se ha reportado que la inmunidad mediada por linfocitos T (LT) juega un papel importante en la defensa de la infección con microsporidios; algunos autores señalan que la respuesta inmune del hospedero contra estos parásitos es del tipo Th1 con producción de IL-2 e INFγ (8)(9)(10)(11)(12)(13)(14)(15)(16)(17).…”

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“…Con relación a la respuesta inmune humoral frente a microsporidios, se ha postulado que los anticuerpos (Ac), aunque juegan un papel importante en el control de la infección, no son suficientes para eliminarla totalmente o prevenir la mortalidad (9,11,13,17). El Fakhry y colaboradores (9) evaluaron mediante las técnicas de ELISA, inmufluorescencia y western blotting la respuesta humoral en ratones silvestres y deficientes para el receptor del IFNg (IFNggR 0/0 ) infectados con E. intestinalis; ambos grupos de ratones desarrollaron la infección que fue crónica en los ratones mutados y transitoria en los silvestres.…”

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Efecto de la ciclosporina A en ratones C57BL/6 infectados con Encephalitozoon intestinalis.

et al. 2006

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Introducción. Encephalitozoon intestinalis es un microsporidio parásito del intestino, que puede diseminarse en pacientes inmunocomprometidos. Existen referencias de modelos animales inmunosuprimidos para el estudio de la microsporidiosis utilizando fármacos que producen supresión total de la respuesta inmune; sin embargo, no se han estudiado los efectos de inmunosupresores con acción selectiva sobre los componentes de esta respuesta. Objetivo. Evaluar el efecto de la inmunosupresión con ciclosporina A (CsA) en ratones C57BL/ 6 infectados con E. intestinalis. Materiales y métodos. Se utilizaron 80 ratones C57BL/6 distribuidos en cuatro grupos: infectados, inmunosuprimidos e infectados, inmunosuprimidos no infectados y controles. La inmunosupresión con CsA (50 mg/kg) se realizó vía intraperitoneal durante todo el estudio. En la semanas 2, 3, 4 y 6 posteriores a la infección se obtuvo sangre para determinar los anticuerpos, y materia fecal para evaluar la cinética de excreción de esporas. Además, se extrajeron varios órganos para estudiar la histopatología y observar la posible diseminación del parásito. Resultados. La producción de anticuerpos IgG fue mayor en los ratones inmunocompetentes infectados que en los inmunosuprimidos infectados con E. intestinalis. No se encontró el parásito en órganos diferentes al intestino delgado en los dos grupos infectados. Sin embargo, la excreción de esporas, tanto en heces como en líquido duodenal, fue mayor en el grupo inmunosuprimido infectado. Conclusión. La CsA en el modelo en ratón no indujo la diseminación de E. intestinalis ni la exacerbación de la enfermedad, pero contribuyó al aumento en la cinética de excreción de esporas y la disminución de la producción de anticuerpos IgG en los ratones inmunosuprimidos infectados.Palabras clave: microsporidios no clasificados, microsporidiosis, formación de anticuerpos, inmunosupresión, ciclosporina. Cyclosporine A effect in mice C57BL/6 infected with Encephalitozoon intestinalis.Introduction. Encephalitozoon intestinalis, a parasite belonging to the phylum Microsporidia, is causes gastrointestinal infections in the immunocompromised host. A suitable pharmacologically immunosuppressed animal model for the study of natural E. intestinalis infection, which can establish the immune components that respond to this parasite, is lacking. Objective. To evaluate the effect of immunosuuppression with Cyclosporine A (CsA) in C57BL/ 6 mice on experimental infection with E.intestinalis infection. Materials and methods. Eighty C57BL/6 mice were distributed in four treatment groups: Control, CsA-immunosuppressed mice without infection, immunocompetent and immunossuppressed mice infected with E. intestinalis. Mice were immunosuppressed with a weekly dose of 50mg/ Kg body weight of CsA, during the course of the study. Five mice from each group were sacrificed 2, 3, 4 and 6 weeks post-infection, to obtain blood for antibody testing and stool samples were analyzed to assess excretion of spores.

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Encephalitozoon intestinalis:Humoral Responses in Interferon-γ Receptor Knockout Mice Infected with a Microsporidium Pathogenic in AIDS Patients

Cited by 42 publications

References 0 publications

Developmental Expression of Two Spore Wall Proteins during Maturation of the Microsporidian Encephalitozoon intestinalis

Developmental Expression of Two Spore Wall Proteins during Maturation of the Microsporidian Encephalitozoon intestinalis

Mammalian Microsporidiosis

Efecto de la ciclosporina A en ratones C57BL/6 infectados con Encephalitozoon intestinalis.

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