<i>Plasmodium yoelii</i> Uses a TLR3-Dependent Pathway to Achieve Mammalian Host Parasitism

Keswani, Tarun; Delcroix-Genete, Delphine; Herbert, Fabien; Leleu, Inès; Lambert, Claire; Draheim, Marion; Salomé‐Desnoulez, Sophie; Saliou, Jean‐Michel; Cazenave, Pierre-André; Silvie, Olivier; Roland, Jacques; Pied, Sylviane

doi:10.4049/jimmunol.1901317

Cited by 2 publications

(2 citation statements)

References 83 publications

(82 reference statements)

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“…These observations strongly suggest a link between the LAP pathway and TLR3-dependent pathway in the transfer of PbA-MVs and the induction of pro-inflammatory cytokine and chemokine responses in astrocytes from CM S mice. Therefore, a TLR3-TRIF-dependent pathway could also participate in neuroinflammation during ECM, similar to what has been reported for the intrahepatic stage [77].…”

Section: Role Of Autophagy-dependent Pmvs In CMsupporting

confidence: 83%

Autophagy Pathways in the Genesis of Plasmodium-Derived Microvesicles: A Double-Edged Sword?

Leleu

Alloo

Cazenave

et al. 2022

Life

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Malaria, caused by Plasmodium species (spp.), is a deadly parasitic disease that results in approximately 400,000 deaths per year globally. Autophagy pathways play a fundamental role in the developmental stages of the parasite within the mammalian host. They are also involved in the production of Plasmodium-derived extracellular vesicles (EVs), which play an important role in the infection process, either by providing nutrients for parasite growth or by contributing to the immunopathophysiology of the disease. For example, during the hepatic stage, Plasmodium-derived EVs contribute to parasite virulence by modulating the host immune response. EVs help in evading the different autophagy mechanisms deployed by the host for parasite clearance. During cerebral malaria, on the other hand, parasite-derived EVs promote an astrocyte-mediated inflammatory response, through the induction of a non-conventional host autophagy pathway. In this review, we will discuss the cross-talk between Plasmodium-derived microvesicles and autophagy, and how it influences the outcome of infection.

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Section: Role Of Autophagy-dependent Pmvs In CMsupporting

confidence: 83%

Autophagy Pathways in the Genesis of Plasmodium-Derived Microvesicles: A Double-Edged Sword?

Leleu

Alloo

Cazenave

et al. 2022

Life

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“…The granulomas damage hepatocytes and the normal histological structure, consequently induce portal hypertension. TLR3 is involved in the host response to viral infection [ 41 ], and has a possible role during Plasmodium infection through the initiation of complex circuits and signals of the immune response [ 42 ]. In this study, gross examination of livers excised indicated that infection caused inflammatory cell infiltration that was no significant difference between WT infected and TLR3 KO infected mice.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of the TLR3 involvement during Schistosoma japonicum-induced pathology

Xie,

Chen,

Feng

et al. 2024

BMC Immunol

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Background Despite the functions of TLRs in the parasitic infections have been extensively reported, few studies have addressed the role of TLR3 in the immune response to Schistosoma japonicum infections. The aim of this study was to investigate the properties of TLR3 in the liver of C57BL/6 mice infected by S. japonicum. Methods The production of TLR3+ cells in CD4+T cells (CD4+CD3+), CD8+T cells (CD8+CD3+), γδT cells (γδTCR+CD3+), NKT cells (NK1.1+CD3+), B cells (CD19+CD3−), NK (NK1.1−CD3+) cells, MDSC (CD11b+Gr1+), macrophages (CD11b+F4/80+), DCs (CD11c+CD11b+) and neutrophils (CD11b+ Ly6g+) were assessed by flow cytometry. Sections of the liver were examined by haematoxylin and eosin staining in order to measure the area of granulomas. Hematological parameters including white blood cell (WBC), red blood cell (RBC), platelet (PLT) and hemoglobin (HGB) were analyzed. The levels of ALT and AST in the serum were measured using biochemical kits. The relative titers of anti-SEA IgG and anti-SEA IgM in the serum were measured by enzyme-linked immunosorbent assay (ELISA). CD25, CD69, CD314 and CD94 molecules were detected by flow cytometry. Results Flow cytometry results showed that the expression of TLR3 increased significantly after S. japonicum infection (P < 0.05). Hepatic myeloid and lymphoid cells could express TLR3, and the percentages of TLR3-expressing MDSC, macrophages and neutrophils were increased after infection. Knocking out TLR3 ameliorated the damage and decreased infiltration of inflammatory cells in infected C57BL/6 mouse livers.,The number of WBC was significantly reduced in TLR3 KO-infected mice compared to WT-infected mice (P < 0.01), but the levels of RBC, platelet and HGB were significantly increased in KO infected mice. Moreover, the relative titers of anti-SEA IgG and anti-SEA IgM in the serum of infected KO mice were statistically decreased compared with the infected WT mice. We also compared the activation-associated molecules expression between S.japonicum-infected WT and TLR3 KO mice. Conclusions Taken together, our data indicated that TLR3 played potential roles in the context of S. japonicum infection and it may accelerate the progression of S. japonicum-associated liver pathology.

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Plasmodium yoelii Uses a TLR3-Dependent Pathway to Achieve Mammalian Host Parasitism

Cited by 2 publications

References 83 publications

Autophagy Pathways in the Genesis of Plasmodium-Derived Microvesicles: A Double-Edged Sword?

Autophagy Pathways in the Genesis of Plasmodium-Derived Microvesicles: A Double-Edged Sword?

Evaluation of the TLR3 involvement during Schistosoma japonicum-induced pathology

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