Gastrointestinal Cell Mediated Immunity and the Microsporidia

Moretto, Magali; Khan, Imtiaz Ali; Weiss, Louis M.

doi:10.1371/journal.ppat.1002775

Cited by 27 publications

(18 citation statements)

References 28 publications

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“…In intraperitoneal E. cuniculi infection models, mice deficient in CD8 + cells or perforin deficient mice have a lethal infection, but there is no lethality in CD4 + deficient mice (32, 37). Oral E. cuniculi infection murine models have shown that CD4+ cells are also involved in the protective immune response for this natural route of infection (33, 38). The most important subset for protective immunity in oral infection models were CD8 + αβ T cells, and dendritic cell IFN-γ protection was critical for priming the gut intraepithelial lymphocyte response (39).…”

Section: Introductionmentioning

confidence: 99%

Microsporidia: Obligate Intracellular Pathogens Within the Fungal Kingdom

2017

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Microsporidia are obligate intracellular pathogens related to Fungi. These organisms have a unique invasion organelle, the polar tube, which upon appropriate environmental stimulation rapidly discharges out of the spore, pierces a host cell’s membrane, and serves as a conduit for sporoplasm passage into the host cell. Phylogenetic analysis suggests that microsporidia are related to the Fungi, being either a basal branch or sister group. Despite the description of microsporidia over 150 years ago, we still lack an understanding of the mechanism of invasion, including the role of various polar tube proteins, spore wall proteins, and host cell proteins in the formation and function of the invasion synapse. Recent advances in ultrastructural techniques are helping to better define the formation and functioning of the invasion synapse. Over the past 2 decades, proteomic approaches have helped define polar tube proteins and spore wall proteins as well as the importance of posttranslational modifications such as glycosylation in the functioning of these proteins, but the absence of genetic techniques for the manipulation of microsporidia has hampered research on the function of these various proteins. The study of the mechanism of invasion should provide fundamental insights into the biology of these ubiquitous intracellular pathogens that can be integrated into studies aimed at treating or controlling microsporidiosis.

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Section: Introductionmentioning

confidence: 99%

Microsporidia: Obligate Intracellular Pathogens Within the Fungal Kingdom

2017

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“…Studies using Encephalitozoon species in mice have helped defined the protective mammalian immune response to microsporidiosis (29,30). Immunity to infection is mediated by T cells and dependent on interferon-gamma (IFN-γ) and interleukin-12 (IL-12) (31)(32)(33)(34). Evidence for this is provided by the protection against lethal microsporidiosis (E. cuniculi infection) afforded by adoptive transfer of sensitized syngenic T-enriched spleen cells into athymic or SCID mice (35,36).…”

Section: Introductionmentioning

confidence: 99%

Microsporidia: Obligate Intracellular Pathogens Within the Fungal Kingdom

Han¹,

Weiss

2017

The Fungal Kingdom

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“…The adaptive immune response is very crucial for containing microsporidiosis. For example, T 195 cells-deficient mice (athymic/nude or SCID) are incapable of successfully killing the pathogen and 196 die due to encephalitozoonosis as opposed to immunocompetent mice (1,26). Similarly, IFN-γ −/− 197 mice lacking major proinflammatory cytokines showed hepatomegaly, colicystitis, splenomegaly, 198…”

Section: Bc) 180mentioning

confidence: 99%

Can immunosuppressed mice control oral infection by the opportunistic pathogenEncephalitozoon intestinalis?

Moura

Alvares-Saraiva

Pérez

et al. 2019

Preprint

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Intestinal mucosa (IM), or the outer surface of the intestine, serves at the primary site for the interaction of various pathogens that cause infection via the oral route. Thus, IM is crucial for developing an efficient adaptive immune response against pathogenic micro-organisms, thereby preventing their colonization and subsequent infection. In the present study, we investigated the immune response to Encephalitozoon intestinalis-caused infection in the IM and gut-associated lymphoid tissue (GALT) in C57BL/6 female mice. To mimic an immunosuppressive condition, the mice were treated with cyclophosphamide (Cy). Histopathology revealed lymphoplasmacytic enteritis at 7 and 14 days-post-infection (dpi) in all infected groups; however, inflammation diminished at 21 and 28 dpi. Cy treatment also led to a higher number of E. intestinalis spores and lesions, which reduced at 28 dpi. In addition, flow cytometry analysis demonstrated CD4+ and CD8+ T cells to be predominant immune cells, with a significant increase in both Th1 and Th2 cytokines at 7 and 14 dpi, as demonstrated by histopathology. In conclusion, Cy treatment reduced GALT (Peyer’s plaques and mesenteric lymph nodes) and peritoneum populations but increased the T-cell population in the intestinal mucosa and the production of pro-inflammatory cytokines, which were able to eliminate this opportunistic fungus and reduced the infection.

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Gastrointestinal Cell Mediated Immunity and the Microsporidia

Cited by 27 publications

References 28 publications

Microsporidia: Obligate Intracellular Pathogens Within the Fungal Kingdom

Microsporidia: Obligate Intracellular Pathogens Within the Fungal Kingdom

Microsporidia: Obligate Intracellular Pathogens Within the Fungal Kingdom

Can immunosuppressed mice control oral infection by the opportunistic pathogenEncephalitozoon intestinalis?

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