Human extracellular vesicles and correlation with two clinical forms of toxoplasmosis

Cruz, Allecinéia Bispo da; Maia, Marta Marques; Pereira, Ingrid de Siqueira; Taniwaki, Noemi Nosomi; Namiyama, Gislene Mitsue; Telles, João Paulo; Vidal, José Ernesto; Spegiorin, Lígia Cosentino Junqueira Franco; Mattos, Cinara Cássia Brandão de; Mattos, Luiz Carlos de; Meira-Strejevitch, Cristina da Silva; Pereira-Chioccola, Vera Lúcia

doi:10.1371/journal.pone.0229602

Cited by 21 publications

(30 citation statements)

References 64 publications

(87 reference statements)

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“…The interaction between both organisms causes the stimulation of host EVs and protective immune response against T gondii derived EVs. These findings were well‐described before 24,36,44 . In addition, T gondii derived EVs used as immunogen caused an immune response capable of reducing the levels of tachyzoites in mouse blood, contributing to parasitaemia reduction and survival indexes increase 27,29,30 …”

Section: Discussionsupporting

confidence: 59%

“…These studies, also, proved that EVs carry pro‐inflammatory factors, including miRNAs, which directly cause the activation of cytokine production 31‐35 . In a previous study, we have shown a significant increase of EVs released in sera of patients with toxoplasmosis (with positive PCR for T gondii ), when they were compared with EV concentration released in sera of healthy individuals 36 . Consequently, high production of EVs could be correlated with the imbalance in immune response.…”

Section: Introductionmentioning

confidence: 82%

“…Concentration (EVs/mL) and size (nm) of murine serum‐derived EVs after ultracentrifugation were evaluated by NTA, using the NanoSight NS300 instrument (Malvern‐NanoSight™, NTA 3.0) as described before 36 . The equipment produced three readings and data were shown as the average and standard deviation of three video recordings of 30‐60 seconds per sample.…”

Section: Methodsmentioning

confidence: 99%

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Characterization of murine extracellular vesicles and Toxoplasma gondii infection

Maia

Cruz

Pereira

et al. 2021

Parasite Immunology

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This study characterized extracellular vesicles (EVs) of sera from mice infected with Toxoplasma gondii or immunized with EVs derived T gondii. EVs were purified of sera from four groups (5 A/Sn mice/group). EV‐IM: Mice immunized with T gondii‐released EVs; ACT: mice in acute infection; CHR: mice in chronic infection; and NI: normal mice. EVs were purified by ultracentrifugation. Concentration of serum‐derived EVs from NI group was smaller than EV‐IM, ACT and CHR groups. Most of the EVs from ACT and CHR groups were microvesicles, and they were bigger than the NI group. The same results were shown by Transmission Electron Microscopy. The presence of exosomes was shown in immunoblotting by tetraspanin (CD63 and CD9) evidence. Splenocytes of EV‐IM, CHR and NI groups were stimulated with T. gondii derived EVs. EV‐IM and CHR groups up‐expressed IFN‐γ; TNF‐α and IL‐17, when compared with the NI group. IL‐10 was up‐expressed only in the EV‐IM group. EV‐IM, ACT and CHR groups expressed more miR‐155‐5p, miR‐29c‐3p and miR‐125b‐5p than the NI group. Host‐T gondii interaction can occur, also, via EVs. miRNAs participate in the modulation of cellular immune response against T gondii. These data give subsidies to propose the differentiation between infect or noninfect hosts by concentration of EVs.

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Section: Discussionsupporting

confidence: 59%

Section: Introductionmentioning

confidence: 82%

Section: Methodsmentioning

confidence: 99%

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Characterization of murine extracellular vesicles and Toxoplasma gondii infection

Maia

Cruz

Pereira

et al. 2021

Parasite Immunology

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“…EV production by some host cells types increases in infectious disease [ 86 , 87 ], and viruses, fungi, bacteria, and parasites have all been shown to directly stimulate host EV production [ 50 , 54 , 55 , 88 ]. A quantitative increase in host EV release has been demonstrated following an extracellular challenge of alveolar epithelial cells with heat-sacrificed bacteria, finding that the elicitor of such response was bacterial CpG DNA binding to endosomal TLR9 receptors [ 85 ].…”

Section: Host Ev-mediated Response To Infectionmentioning

confidence: 99%

The complex, bidirectional role of extracellular vesicles in infection

White

Dauros-Singorenko

Hong

et al. 2021

Biochemical Society Transactions

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Cells from all domains of life release extracellular vesicles (EVs), packages that carry a cargo of molecules that participate in communication, co-ordination of population behaviours, virulence and immune response mechanisms. Mammalian EVs play an increasingly recognised role to fight infection, yet may also be commandeered to disseminate pathogens and enhance infection. EVs released by bacterial pathogens may deliver toxins to host cells, signalling molecules and new DNA to other bacteria, and act as decoys, protecting infecting bacteria from immune killing. In this review, we explore the role of EVs in infection from the perspective of both the pathogen and host, and highlight their importance in the host/pathogen relationship. We highlight proposed strategies for EVs in therapeutics, and call attention to areas where existing knowledge and evidence is lacking.

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“…TEM and NTA analysis identified vesicles with circular or elliptical vesicular structures ranging from 50 to 200 nm in diameter, the shape and size of which were similar to those described in our previous study and to those released by other helminths [ 14 ], such as Taenia asiatica , Echinococcus granulosus , and Echinococcus multilocularis [ 12 , 20 , 25 ]. The transmembrane proteins CD9 and CD63 are considered as exosomal markers and are frequently used to identify exosomes after isolation [ 26 , 27 ]. Our ITEM analysis results showed that CD9 and CD63 were detected in exosome-like vesicles from T. pisiformis metacestodes.…”

Section: Discussionmentioning

confidence: 99%

Exosomal microRNA let-7-5p from Taenia pisiformis Cysticercus Prompted Macrophage to M2 Polarization through Inhibiting the Expression of C/EBP δ

et al. 2021

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Cysticercus pisiformis, the larval stage of Taenia pisiformis, causes serious illness in rabbits that severely impacts the rabbit breeding industry. An inhibitive Th2 immune response can be induced by let-7-enriched exosomes derived from T. pisiformis cysticercus. However, the underlying molecular mechanisms are not completely understood. Here, we report that exosomal miR-let-7-5p released by T. pisiformis cysticercus played a critical role in the activation of M2 macrophages. We found that overexpression of let-7-5p in M1 macrophages decreased M1 phenotype expression while promoting polarization to the M2 phenotype, which is consistent with experimental data in exosome-treated macrophages alone. In contrast, knockdown of let-7-5p in exosome-like vesicles promoted M1 polarization and decreased M2 phenotype expression. Furthermore, down-regulation of transcription factor CCAAT/enhancer-binding protein (C/EBP)-δ resulted in the decrease of M1 phenotype markers and increase of M2 phenotype markers. These results suggested that let-7 enriched in exosome-like vesicles from T. pisiformis metacestodes can induce M2 macrophage polarization via targeting C/EBP δ, which may be involved in macrophage polarization induced by T. pisiformis metacestodes. The finding helps to expand our knowledge of the molecular mechanism of immunosuppression and Th2 immune response induced by metacestodes.

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Human extracellular vesicles and correlation with two clinical forms of toxoplasmosis

Abstract: AimThis study analyzed microvesicles and exosomes, called as extracellular vesicles (EVs) excreted in serum and cerebrospinal fluid (CSF) from patients with cerebral or gestational toxoplasmosis.

Cited by 21 publications

References 64 publications

Characterization of murine extracellular vesicles and Toxoplasma gondii infection

Characterization of murine extracellular vesicles and Toxoplasma gondii infection

The complex, bidirectional role of extracellular vesicles in infection

Exosomal microRNA let-7-5p from Taenia pisiformis Cysticercus Prompted Macrophage to M2 Polarization through Inhibiting the Expression of C/EBP δ

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