Immune response to Encephalitozoon infection review

Valenčáková, Alexandra; Halánová, Monika

doi:10.1016/j.cimid.2011.11.004

Cited by 36 publications

(39 citation statements)

References 43 publications

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“…When the T-cell count falls below 100/µl blood, infection manifests itself as acute microsporidiosis, often with systemic involvement [17], [32]. Over the decades, several reviews on non-specific and adaptive immune responses involved in the fight against microsporidial infection have been published [33]–[35]. It is generally accepted that a protective immune response against this parasite is mediated by cytotoxic CD8+ T-lymphocytes [36] and their activation does not appear to be dependent upon CD4+ T-cells [37], [38].…”

Section: Discussionmentioning

confidence: 99%

Latent Microsporidiosis Caused by Encephalitozoon cuniculi in Immunocompetent Hosts: A Murine Model Demonstrating the Ineffectiveness of the Immune System and Treatment with Albendazole

et al. 2013

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BackgroundMicrosporidia are obligate intracellular parasites causing severe infections with lethal outcome in immunocompromised hosts. However, these pathogens are more frequently reported as latent infections in immunocompetent individuals and raises questions about the potential risk of reactivation following induced immunosuppression.AimsTo evaluate the possibility latent microsporidiosis, efficacy or albendazole, and reactivation, the authors monitored the course of E. cuniculi infection in immunocompetent BALB/c mice and immunodeficient SCID mice using molecular methods.MethodsMice were per orally infected with 107 spores of E. cuniculi. Selected groups were treated with albendazole, re-infected or chemically immunosuppressed by dexamethasone. The presence of microsporidia in the host’s organs and feces were determined using PCR methods. Changes in numbers of lymphocytes in blood and in spleen after induction of immunosuppression were confirmed using flow cytometry analysis.ResultsWhereas E. cuniculi caused lethal microsporidiosis in SCID mice, the infection in BABL/c mice remained asymptomatic despite parasite dissemination into many organs during the acute infection phase. Albendazole treatment led to microsporidia elimination from organs in BALB/c mice. In SCID mice, however, only a temporary reduction in number of affected organs was observed and infection re-established post-treatment. Dexamethasone treatment resulted in a chronic microsporidia infection disseminating into most organs in BALB/c mice. Although the presence of E. cuniculi in organs of albendazole- treated mice was undetectable by PCR, it was striking that infection was reactivated by immunosuppression treatment.ConclusionOur results demonstrated that microsporidia can successfully survive in organs of immunocompetent hosts and are able to reactivate from undetectable levels and spread within these hosts after induction of immunosuppression. These findings stress the danger of latent microsporidiosis as a life-threatening risk factor especially for individuals undergoing chemotherapy and in transplant recipients of organs originating from infected donors.

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Section: Discussionmentioning

confidence: 99%

Latent Microsporidiosis Caused by Encephalitozoon cuniculi in Immunocompetent Hosts: A Murine Model Demonstrating the Ineffectiveness of the Immune System and Treatment with Albendazole

et al. 2013

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“…İmmunocompetent bireylerde mikrosporidia'ya karşı IgM ve IgG antikorları gelişmekte ve yaşam boyu devam etmektedir. İmmunsupresif bireylerde ise antikor yanıtı değişkendir (15,58).…”

Section: Immüniteunclassified

“…CD4 + ve CD8 + hücreleri enfeksiyona karşı dirençte önemli olup, CD8 + T hücreleri hücre içi enfeksiyonlarda önemli rol oynamakta ve parazit replikasyonunu kontrol etmektedir. E. cuniculi enfeksiyonlarında CD8 + T lenfositlerinin konağın korunmasında ve uzun süreli bir immün yanıtın oluşmasında önemli rol oynadığı bildirilmektdir (58).…”

Section: Immüniteunclassified

Mikrosporidialar ve Mikrosporidiyozis

Yazar¹,

Koru²,

Hamamcı³

et al. 2013

TurkiyeParazitolDerg

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ÖZETMikrosporidialar, zorunlu hücre içi parazitidirler ve konak hücresi dışında metabolik aktivasyon göstermemektedirler. Ökaryotik hücrelerdir, fakat bazı tipik ökaryotik özellikler eksiktir. Şimdiye kadar tanımlamış 144 cins içinde 1200'den fazla türü vardır. Mikrosporidiaların en çok bilinene evresi küçük ve oldukça dirençli olan sporlarıdır. Boyutları türe göre farklılık gösterir ama genellikle 1-10 µm arasındadır. Mikrosporodiaların hayatları üç fazda incelenebilir; enfektif veya çevresel faz, proliferatif veya üreme fazı ve sporogonik faz. Mikrosporidiaların tanısında Işık mikroskobu, Transmisyon Elektron Mikroskobu (TEM), Immünofloresan tekniği (IFA) ve Moleküler yöntemler gibi değişik metotlar kullanılmaktadır. Klinik semptomlar, enfeksiyonun lokalizasyonu ve konağın immün durumu ile yakından ilişkilidir. İnsanlarda görülen mikrosporidiosis önemli ve hızlı gelişen fırsatçı bir hastalıktır özellikle de AIDS'li immunocompromise hastalarda daha ciddi seyretmektedir. Mikrosporidiosis'in tedavisi genellikle ilaç ve destek tedavi ile sağlanmaktadır. Enfeksiyona ve türüne bağlı olarak farklı ilaçlar kullanılmaktadır. Tedavide en yaygın olarak albendazol ve fumagilin kullanıldığı belirtilmektedir. (Turkiye Parazitol Derg 2013; 37: 123-34) Anahtar Sözcükler: Mikrosporidia, mikrosporidiyozis, tanı yöntemleri, klinik Geliş Tarihi: 02.01.2013Kabul Tarihi: 19.02.2013 ABSTRACTAll microsporidia are obligate parasites and have no active stages outside their host cells. Microsporidia lack some typical eukaryotic characteristics. There are now over 1200 species identified in 144 genera. The most familiar stage of microsporidia is the small, highly resistant spore, the size of which differs according to the species and is often 1-10 µm. The general life cycle pattern of the microsporidia can be divided into three phases: the infective or environmental phase, the proliferative phase, and the sporogony or spore-forming phase. There are several methods for diagnosing microsporidia: light microscopic, transmission electron microscopy (TEM), immunofluorescence assays (IFA) and molecular methods. The clinical course of microsporidiosis depends on the immune status of the host and site of infection. Microsporidia can cause infections such as diarrhoea, keratitis, myositis, bronchitis and brochiolitis. Human microsporidiosis represents an important and rapidly emerging opportunistic disease, occurring mainly, but not exclusively, in severely immunocompromised patients with AIDS. The treatment of microsporidiosis is generally achieved with medications and supportive care. Depending on the site of infection and the microsporidia species involved, different medications are utilized. The most commonly used medications for microsporidiosis include albendazole and fumagillin. (Turkiye Parazitol Derg 2013; 37: 123-34)

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“…These populations include mostly HIV infected and patients in chemotherapy [4,5]. In decreased immune response, the pathogen development and spreads are facilitate determining cells death [6,7,8,9]. However, a previous study in mice infected with E. cuniculi showed that even in animals treated with albendazole the pathogen could reinfect, characterizing a latent infection [10].…”

Section: Introductionmentioning

confidence: 99%

Cyclophosphamide immunosuppressed Xid mice model clarify the protective role of B cells in experimental encephalitozoonosis

Crs

et al. 2018

Preprint

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21Encephalitozoon cuniculi is an intracellular pathogen that stablishes a balanced relationship 22 with immunocompetent individuals, which is dependent of T lymphocytes activity. We 23 previously showed X-linked immunodeficiency (XID -B cell deficient) mice are more 24 susceptible to encephalitozoonosis and B-1 cells presence influences in the immune response. 25 Because XID mice are deficient both in B-1 and B-2 cells, here we investigate the role of these 26 cells against E. cuniculi infection using cyclophosphamide (Cy) immunosuppressed murine 27 model to exacerbate the infection. XID mice presented lethargy and severe symptoms, 28 associated with encephalitozoonosis and there was an increase in the peritoneal populations of 29 CD8 + and CD4 + T lymphocytes and macrophages and also in the proinflammatory cytokines 30 IFN-γ, TNF-α and IL-6. In BALB/c mice, no clinical signs were observed and there was an 31 increase of T lymphocytes and macrophages in the spleen, showing an effective immune 32 response. B-2 cells transfer to XID mice resulted in reduction of symptoms and lesion area with 33 increase of B-2 and CD4 + T populations in the spleen. B-1 cells transfer increased the peritoneal 34 populations of B-2 cells and macrophages and also reduced the symptoms. Therefore, the 35 immunodeficiency of B cells associated to Cy immunosuppression condition leads to 36 disseminated and severe encephalitozoonosis in XID mice with absence of splenic immune 37 response and ineffective local immune response, evidencing the B-1 and B-2 cells role against 38 microsporidiosis.39 40 lymphocytes 42 43 3 44 Author summary 45 46 The adaptive immune response plays a key role against Encephalitozoon cuniculi, an 47 opportunistic fungus for T cells immunodeficient patients. The role of B cells and antibody play 48 in natural resistance to Encephalitozoon cuniculi remains unresolved. Previously, we 49 demonstrated that B-1 deficient mice (XID), an important component of innate immunity, were 50 more susceptible to encephalitozoonosis, despite the increase in the number of CD4 + and CD8 + 51 T lymphocytes. In order to better understand the role of B-1 and B-2 cells and the relationship 52 with the other cells of the immune response in encephalitozoonosis, we infected with E. cuniculi 53 in cyclophosphamide immunosuppressed mice. Here we demonstrate that infected XID mice 54 showed reduction of T cells and macrophages and increase of proinflammatory cytokines 55 associated with disseminated and severe encephalitozoonosis with presence of abdominal 56 effusion and lesions in multiple organs. This pattern of infection observed in mice with genetic 57 deficiency in T cells, so we suggest that the absence of B-1 cells affects the cytotoxic capacity 58 of these lymphocytes. When we transfer B-2 cells to XID mice, the lesion areas caused by the 59 fungus, the populations of T lymphocytes in the peritoneum and the proinflammatory cytokines 60 decrease, indicating a better resolution of the infection. We speculate that B-1 and B-2 cells...

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Immune response to Encephalitozoon infection review

Cited by 36 publications

References 43 publications

Latent Microsporidiosis Caused by Encephalitozoon cuniculi in Immunocompetent Hosts: A Murine Model Demonstrating the Ineffectiveness of the Immune System and Treatment with Albendazole

Latent Microsporidiosis Caused by Encephalitozoon cuniculi in Immunocompetent Hosts: A Murine Model Demonstrating the Ineffectiveness of the Immune System and Treatment with Albendazole

Mikrosporidialar ve Mikrosporidiyozis

Cyclophosphamide immunosuppressed Xid mice model clarify the protective role of B cells in experimental encephalitozoonosis

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