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1.
Trends Parasitol ; 36(2): 87-90, 2020 02.
Artigo em Inglês | MEDLINE | ID: mdl-31753545

RESUMO

Helminth infections can activate multimeric protein complexes called inflammasomes. In this forum we summarize the main effects of the NLRP3 inflammasome activation, including control of excessive Th2 response and immunopathology induction. These mechanisms would ensure the survival of both the host and the parasite.


Assuntos
Helmintíase/imunologia , Helmintíase/parasitologia , Helmintos/imunologia , Interações Hospedeiro-Parasita/imunologia , Inflamassomos/imunologia , Proteína 3 que Contém Domínio de Pirina da Família NLR/imunologia , Animais , Humanos
2.
Front Immunol ; 11: 2087, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-33193292

RESUMO

Fasciola hepatica is helminth parasite found around the world that causes fasciolosis, a chronic disease affecting mainly cattle, sheep, and occasionally humans. Triclabendazole is the drug of choice to treat this parasite. However, the continuous use of this drug has led to the development of parasite resistance and, consequently, the limitation of its effectiveness. Hence, vaccination appears as an attractive option to develop. In this work, we evaluated the potential of F. hepatica Kunitz-type molecule (FhKTM) as an antigen formulated with a liquid crystal nanostructure formed by self-assembly of 6-O-ascorbyl palmitate ester (Coa-ASC16) and the synthetic oligodeoxynucleotide containing unmethylated cytosine-guanine motifs (CpG-ODN) during an experimental model of fasciolosis in mice, and we further dissected the immune response associated with host protection. Our results showed that immunization of mice with FhKTM/CpG-ODN/Coa-ASC16 induces protection against F. hepatica challenge by preventing liver damage and improving survival after F. hepatica infection. FhKTM/CpG-ODN/Coa-ASC16-immunized mice elicited potent IFN-γ and IL-17A with high levels of antigen-specific IgG1, IgG2a, and IgA serum antibodies. Strikingly, IL-17A blockade during infection decreased IgG2a and IgA antibody levels as well as IFN-γ production, leading to an increase in mortality of vaccinated mice. The present study highlights the potential of a new vaccine formulation to improve control and help the eradication of F. hepatica infection, with potential applications for natural hosts such as cattle and sheep.


Assuntos
Anticorpos Anti-Helmínticos/imunologia , Fasciola hepatica/imunologia , Fasciolíase/prevenção & controle , Proteínas de Helminto/farmacologia , Interferon gama/imunologia , Interleucina-17/imunologia , Vacinas/farmacologia , Animais , Fasciolíase/imunologia , Feminino , Proteínas de Helminto/imunologia , Camundongos , Camundongos Endogâmicos BALB C , Vacinas/imunologia
3.
Front Immunol ; 10: 552, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-30967874

RESUMO

The production of IL-1-family cytokines such as IL-1ß and IL-18 is finely regulated by inflammasome activation after the recognition of pathogens associated molecular pattern (PAMPs) and danger associated molecular patterns (DAMPs). However, little is known about the helminth-derived molecules capable of activating the inflammasome. In the case of the helminth trematode Fasciola hepatica, the secretion of different cathepsin L cysteine peptidases (FhCL) is crucial for the parasite survival. Among these enzymes, cathepsin L3 (FhCL3) is expressed mainly in the juvenile or invasive stage. The ability of FhCL3 to digest collagen has demonstrated to be critical for intestinal tissue invasion during juvenile larvae migration. However, there is no information about the interaction of FhCL3 with the immune system. It has been shown here that FhCL3 induces a non-canonical inflammasome activation in dendritic cells (DCs), leading to IL-1ß and IL-18 production without a previous microbial priming. Interestingly, this activation was depending on the cysteine protease activity of FhCL3 and the NLRP3 receptor, but independent of caspase activation. We also show that FhCL3 is internalized by DCs, promoting pro-IL-1ß cleavage to its mature and biologically active form IL-1ß, which is released to the extracellular environment. The FhCL3-induced NLRP3 inflammasome activation conditions DCs to promote a singular adaptive immune response, characterized by increased production of IFN-γ and IL-13. These data reveal an unexpected ability of FhCL3, a helminth-derived molecule, to activate the NLRP3 inflammasome, which is independent of the classical mechanism involving caspase activation.


Assuntos
Catepsina L/imunologia , Células Dendríticas/imunologia , Fasciola hepatica/imunologia , Proteínas de Helminto/imunologia , Inflamassomos/imunologia , Proteína 3 que Contém Domínio de Pirina da Família NLR/imunologia , Animais , Inflamassomos/genética , Interleucina-18/genética , Interleucina-18/imunologia , Interleucina-1beta/genética , Interleucina-1beta/imunologia , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Knockout , Proteína 3 que Contém Domínio de Pirina da Família NLR/genética
4.
Front Immunol ; 9: 664, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-29670630

RESUMO

The survival of helminths in the host over long periods of time is the result of a process of adaptation or dynamic co-evolution between the host and the parasite. However, infection with helminth parasites causes damage to the host tissues producing the release of danger signals that induce the recruitment of various cells, including innate immune cells such as macrophages (Mo), dendritic cells (DCs), eosinophils, basophils, and mast cells. In this scenario, these cells are able to secrete soluble factors, which orchestrate immune effector mechanisms that depend on the different niches these parasites inhabit. Here, we focus on recent advances in the knowledge of excretory-secretory products (ESP), resulting from helminth recognition by DCs and Mo. Phagocytes and other cells types such as innate lymphocyte T cells 2 (ILC2), when activated by ESP, participate in an intricate cytokine network to generate innate and adaptive Th2 responses. In this review, we also discuss the mechanisms of innate immune cell-induced parasite killing and the tissue repair necessary to assure helminth survival over long periods of time.


Assuntos
Células Dendríticas/imunologia , Helmintíase/imunologia , Helmintos/fisiologia , Imunidade Inata , Macrófagos/imunologia , Fagócitos/imunologia , Células Th2/imunologia , Animais , Interações Hospedeiro-Parasita , Humanos , Imunomodulação , Moléculas com Motivos Associados a Patógenos/imunologia
5.
Semin Immunopathol ; 39(2): 199-213, 2017 02.
Artigo em Inglês | MEDLINE | ID: mdl-27587063

RESUMO

The effective defense against parasite infections requires the ability to mount an appropriate and controlled specific immune response able to eradicate the invading pathogen while limiting the collateral damage to self-tissues. Dendritic cells are key elements for the development of immunity against parasites; they control the responses required to eliminate these pathogens while maintaining host homeostasis. Ligation of dendritic cell pattern recognition receptors by pathogen-associated molecular pattern present in the parasites initiates signaling pathways that lead to the production of surface and secreted proteins that are required, together with the antigen, to induce an appropriate and timely regulated immune response. There is evidence showing that parasites can influence and regulate dendritic cell functions in order to promote a more permissive environment for their survival. In this review, we will focus on new insights about the ability of protozoan and helminth parasites or their products to modify dendritic cell function and discuss how this interaction is crucial in shaping the host response.


Assuntos
Células Dendríticas/imunologia , Células Dendríticas/metabolismo , Interações Hospedeiro-Parasita/imunologia , Parasitos/imunologia , Doenças Parasitárias/imunologia , Doenças Parasitárias/metabolismo , Animais , Humanos , Sistema Imunitário/citologia , Sistema Imunitário/imunologia , Sistema Imunitário/metabolismo , Tolerância Imunológica , Janus Quinases/metabolismo , Doenças Parasitárias/parasitologia , Fatores de Transcrição STAT/metabolismo , Transdução de Sinais , Subpopulações de Linfócitos T/imunologia , Subpopulações de Linfócitos T/metabolismo , Receptores Toll-Like/metabolismo
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