Microsporidia and acquired immunodeficiency syndrome

Schottelius, Justus Georg; Costa, Salvatore

doi:10.1590/s0074-02762000000700022

Cited by 10 publications

(9 citation statements)

References 52 publications

(25 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Microsporidiosis has been reported as the cause of chronic and life-threatening diseases in human immunodeficiency virus/ AIDS patients and organ recipients and, therefore, has gained a greater medical importance among individuals who have an impaired immune status (4,8,32,36). Increasingly, infections involving immunocompetent individuals, particularly those affecting the elderly or young, have also been reported (8,10,24,31).…”

mentioning

confidence: 99%

“…Infections are believed to occur primarily through the ingestion of microsporidian spores and proceed through the invasion of enterocytes in the small intestine (8). Clinical reports of microsporidiosis have described a range in the severity of the disease, from intestinal infections leading to chronic diarrhea to disseminated diseases thought to occur as a result of migrating macrophages, including keratoconjunctivitis, sinusitis, tracheobronchitis, encephalitis, interstitial nephritis, hepatitis, cholecystitis, osteomyelitis, and myositis (8,18,32,36).…”

mentioning

confidence: 99%

See 1 more Smart Citation

Toll-Like Receptor 2 Recognition of the MicrosporidiaEncephalitozoonspp. Induces Nuclear Translocation of NF-κB and Subsequent Inflammatory Responses

2008

View full text Add to dashboard Cite

Microsporidia are obligate intracellular parasites that are ubiquitous in nature and have been recognized as causing an important emerging disease among immunocompromised individuals. Limited knowledge exists about the immune response against these organisms, and virtually nothing is known about the receptors involved in host recognition. Toll-like receptors (TLR) are pattern recognition receptors that bind to specific molecules found on pathogens and signal a variety of inflammatory responses. In this study, we show that both Encephalitozoon cuniculi and Encephalitozoon intestinalis are preferentially recognized by TLR2 and not by TLR4 in primary human macrophages. This is the first demonstration of host receptor recognition of any microsporidian species. TLR2 ligation is known to activate NF-B, resulting in inflammatory cytokines, such as tumor necrosis factor alpha (TNF-␣) and interleukin-8 (IL-8). We found that the infection of primary human macrophages leads to the nuclear translocation of NF-B in as early as 1 h and the subsequent production of TNF-␣ and IL-8. To verify the direct role of TLR2 parasite recognition in the production of these cytokines, the receptor was knocked down in primary human macrophages using small interfering RNA. This knockdown resulted in decreases in both the nuclear translocation of NF-B and the levels of TNF-␣ and IL-8 after challenge with spores. Taken together, these experiments directly link the initial inflammatory response induced by Encephalitozoon spp. to TLR2 stimulation in human macrophages.

show abstract

mentioning

confidence: 99%

mentioning

confidence: 99%

Toll-Like Receptor 2 Recognition of the MicrosporidiaEncephalitozoonspp. Induces Nuclear Translocation of NF-κB and Subsequent Inflammatory Responses

2008

View full text Add to dashboard Cite

show abstract

“…Recientemente, varios miembros del filo Microsporidia (3) se han descrito como parásitos en humanos (1,2,(4)(5)(6)(7). Sin embargo, solamente dos especies, Encephalitozoon intestinalis y Enterocytozoon bieneusi, se han reconocido como microsporidios intestinales, principalmente en hospederos inmunocomprometidos afectados por el síndrome de inmunodeficiencia adquirida y en pacientes trasplantados.…”

unclassified

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

et al. 2006

View full text Add to dashboard Cite

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.

show abstract

“…Some opportunistic organisms as Microsporidia have been underestimated (Schottelius & Gonçalves da Costa 2000) and prevalence of this and other opportunistic microorganisms or parasites tends raised since accurate diagnostic methods will be applicated.…”

mentioning

confidence: 99%

Immunocompromised host: from the early events until the impact of acquired immunodeficiency syndrome

Costa¹

2000

Mem. Inst. Oswaldo Cruz

View full text Add to dashboard Cite

Microsporidia and acquired immunodeficiency syndrome

Abstract: Microsporidia is a common term that has been used to refer to

Cited by 10 publications

References 52 publications

Toll-Like Receptor 2 Recognition of the MicrosporidiaEncephalitozoonspp. Induces Nuclear Translocation of NF-κB and Subsequent Inflammatory Responses

Toll-Like Receptor 2 Recognition of the MicrosporidiaEncephalitozoonspp. Induces Nuclear Translocation of NF-κB and Subsequent Inflammatory Responses

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

Immunocompromised host: from the early events until the impact of acquired immunodeficiency syndrome

Contact Info

Product

Resources

About