Advancement in our understanding of immune response against <i>Encephalitozoon</i> infection

Aseeja, Praisy; Shaikh, Yasmin; Bajpai, Anamika; Sirsikar, Prachitee; Kalra, Samir Kumar

doi:10.1111/pim.12828

Cited by 5 publications

(4 citation statements)

References 107 publications

(181 reference statements)

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“…E. cuniculi parasites are indeed described as hackers of host innate immune defenses ( Dalboni et al, 2021 ). They escape Mo immunity by inhibiting phagolysosomal fusion or by germinating directly into the cytoplasm of these cells ( Franzen and Müller, 2001 ; Aseeja et al, 2021 ). They also favor efferocytosis and polarize Mo to an M2 profile, facilitating their survival and multiplication inside these cells ( Pereira et al, 2019 ; Dalboni et al, 2021 ).…”

Section: Introductionmentioning

confidence: 99%

A mouse ear skin model to study the dynamics of innate immune responses against the microsporidian Encephalitozoon cuniculi

et al. 2023

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Microsporidia are obligate intracellular parasites related to fungi that cause severe infections in immunocompromised individuals. Encephalitozoon cuniculi is a microsporidian species capable of infecting mammals, including human and rodents. In response to microsporidian infection, innate immune system serves as the first line of defense and allows a partial clearance of the parasite via the innate immune cells, namely macrophages, neutrophils, dendritic cells, and Natural Killer cells. According to the literature, microsporidia bypass this response in vitro by modulating the response of macrophages. In order to study host-parasites interactions in vivo, we developed a model using the mouse ear pinna in combination with an intravital imaging approach. Fluorescent E. cuniculi spores were inoculated into the skin tissue to follow for the first time in real time in an in vivo model the recruitment dynamics of EGFP + phagocytic cells in response to the parasite. The results show that parasites induce an important inflammatory recruitment of phagocytes, with alterations of their motility properties (speed, displacement length, straightness). This cellular response persists in the injection zone, with spores detected inside the phagocytes up to 72 h post-infection. Immunostainings performed on ear tissue cryosections evoke the presence of developing infectious foci from 5 days post-infection, in favor of parasite proliferation in this tissue. Overall, the newly set up mice ear pinna model will increase our understanding of the immunobiology of microsporidia and in particular, to know how they can bypass and hijack the host immune system of an immunocompetent or immunosuppressed host.

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Section: Introductionmentioning

confidence: 99%

A mouse ear skin model to study the dynamics of innate immune responses against the microsporidian Encephalitozoon cuniculi

et al. 2023

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“…It infects epithelial and endothelial cells, fibroblasts, and macrophages of various mammals, including rabbits, rodents, carnivores, monkeys, several wild mammals, and humans [6]. Several researchers have evaluated immunity against microsporidia, especially E. cuniculi , in recent years, and highlighted the importance of adaptive immunity in combating microsporidiosis [7, 8]. T cells protect against E. cuniculi infection [9, 10, 11].…”

Section: Introductionmentioning

confidence: 99%

“…Several researchers have evaluated immunity against microsporidia, especially E. cuniculi, in recent years, and highlighted the importance of adaptive immunity in combating microsporidiosis [7,8]. T cells protect against E. cuniculi infection [9,10,11].…”

Section: Introductionmentioning

confidence: 99%

Contribution of B-1 cells in the cytotoxicity of CD8 T lymphocytes in encephalitozoonosis

de Oliveira,

Perez,

Alvares-Saraiva

et al. 2023

Preprint

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Encephalitozoon cuniculiis an opportunistic intracellular pathogen that establishes a balanced relationship with immunocompetent individuals depending on the activity of their CD8+T cells lymphocytes. However, lower resistance to experimental infection withE. cuniculiwas found in B-1 deficient mice (Xid), besides increased the number of CD8 T lymphocytes. Here, we evaluated the cytotoxic activity of CD8+T lymphocytes from Balb/c wild-type (WT) or Balb/c Xid mice (with B-1 cell deficiency) on the microbicidal activity of macrophages challenged withE. cuniculi. CD8 T lymphocytes from WT or Xid mice previously infected or not withE cuniculiwere co-cultured with macrophages challenged withE. cuniculi. We evaluated macrophages viability and microbicidal activity, and proliferation, viability, and presence of activating molecules (CD62L, CD69, and CD107a) in CD8 T lymphocytes. Macrophages co-cultured with CD8 T lymphocytes from WT demonstrated high microbicidal activity. CD8 T lymphocytes obtained from uninfected WT mice had a higher proliferative capacity and a higher expression of CD69 and LAMP-1-activating molecules compared to Xid CD8+T lymphocytes. CD8 T lymphocytes from infected Xid mice proliferated more than those from WT mice, however, when the expression of the activating molecule CD69 associated with the expression of CD62L was kept low. In conclusion, the absence of B-1 cells in Xid mice might be associated with the lower expression of activating molecules in CD8+T lymphocytes and their cytotoxic activity. However, after a previous infection withE. cuniculi, CD8 T lymphocytes were more effective in killing macrophages infected withE. cuniculi.

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“…Since the first report of human microsporidian infections was been known in 1959 [5], the research on microsporidiosis has attracted much more attention. Now we know that the host innate immunity plays a significant role against microsporidia, such as the interactions between microsporidia and macrophages [6][7][8]. As key regulators of innate immunity and inflammation, monocytes and macrophages mainly play a role in pathogen clearance, antigen presenting, induction of adaptive immune response and so on [9].…”

Section: Introductionmentioning

confidence: 99%

Encephalitozoon hellem Infection Promotes Monocytes Extravasation

Wang

et al. 2022

Pathogens

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Background: Microsporidia are a group of obligated intracellular fungus pathogens. Monocytes and the derivative macrophages are among the most important players in host immunity. The invasion of microsporidia may significantly affect the monocytes maturation and extravasation processes. Methods: We utilized a previously established microsporidia infection murine model to investigate the influences of microsporidia Encephalitozoon hellem (E. hellem) infection on monocyte maturation, releasing into the circulation and extravasation to the inflammation site. Flow cytometry and qPCR analysis were used to compare the monocytes and derivative macrophages isolated from bone marrow, peripheral blood and tissues of E. hellem-infected and control mice. Results: The results showed that the pro-inflammatory group of CD11b+Ly-6C+ monocytes are promoted in E. hellem-infected mice. Interestingly, the percentage of Ly-6C+ monocytes from E. hellem-infected mice are significantly lower in peripheral blood while significantly higher in the inflamed small intestine, together with up-regulated ratio of F4/80 macrophage in small intestine as well. Conclusions: Our findings demonstrated that E. hellem infection leads to promoted monocytes maturation in bone marrow, up-regulation of extravasation from peripheral blood to inflammation site and maturation into macrophages. Our study is the first systematic analysis of monocytes maturation and trafficking during microsporidia infection, and will provide better understanding of the pathogen–host interactions.

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Advancement in our understanding of immune response against Encephalitozoon infection

Cited by 5 publications

References 107 publications

A mouse ear skin model to study the dynamics of innate immune responses against the microsporidian Encephalitozoon cuniculi

A mouse ear skin model to study the dynamics of innate immune responses against the microsporidian Encephalitozoon cuniculi

Contribution of B-1 cells in the cytotoxicity of CD8 T lymphocytes in encephalitozoonosis

Encephalitozoon hellem Infection Promotes Monocytes Extravasation

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