Insights into anti-parasitism induced by a C-type lectin from Bothrops pauloensis venom on Toxoplasma gondii

Castanheira, Letícia Eulalio; Souza, Dayane Lorena Naves de; Silva, Rafaela José; Barbosa, Bellisa Freitas; Mineo, José Roberto; Tudini, Kelly Aparecida; Rodrigues, Renata Santos; Ferro, Eloísa Amália Vieira; Ávila, Veridiana de Melo Rodrigues

doi:10.1016/j.ijbiomac.2014.11.035

Cited by 30 publications

(18 citation statements)

References 44 publications

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“…C-type lectin signaling pathway is another pathway that links innate immune response and adaptive immune response. Two recent reports showed that C-type lectin can restrict T. gondii parasitism [ 33 , 34 ]. In the present study, ten C-type lectin molecules were differentially expressed, including eight upregulated C-type lectins (Clec12a, Clec1b, Clec4a1, Clec4a2, Clec4a3, Clec4e, Clec4n and Clec7a) and two downregulated C-type lectins (Clec11a and Clec3b).…”

Section: Discussionmentioning

confidence: 99%

Transcriptomic analysis of mouse liver reveals a potential hepato-enteric pathogenic mechanism in acute Toxoplasma gondii infection

Elsheikha

et al. 2016

Parasites Vectors

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BackgroundToxoplasma gondii is a worldwide spread pathogen which can infect all tissues of its host. The transcriptomic responses of infected brain and spleen have been reported. However, our knowledge of the global transcriptomic change in infected liver is limited. Additionally, T. gondii infection represents a highly dynamic process involving complex biological responses of the host at many levels. Herein, we describe such processes at a global level by discovering gene expression changes in mouse livers after acute infection with T. gondii ToxoDB#9 strain.ResultsGlobal transcriptomic analysis identified 2,758 differentially expressed transcripts in infected liver, of which 1,356 were significantly downregulated and 1,402 upregulated. GO and KEGG database analyses showed that host immune responses were upregulated, while the metabolic-related processes/pathways were downregulated, especially xenobiotic metabolism, fatty acid metabolism, energy metabolism, and bile biosynthesis and secretion. The metabolism of more than 800 chemical compounds including anti-Toxoplasma prescribed medicines were predicted to be modulated during acute T. gondii infection due to the downregulation of enzymes involved in xenobiotic metabolism.ConclusionsTo the best of our knowledge, this is the first global transcriptomic analysis of mouse liver infected by T. gondii. The present data indicate that during the early stage of liver infection, T. gondii can induce changes in liver xenobiotic metabolism, upregulating inflammatory response and downregulating hepatocellular PPAR signaling pathway, altering host bile biosynthesis and secretion pathway; these changes could enhance host intestinal dysbacteriosis and thus contribute to the pathological changes of both liver and intestine of infected mice. These findings describe the biological changes in infected liver, providing a potential mechanistic pathway that links hepatic and intestinal pathologies to T. gondii infection.Electronic supplementary materialThe online version of this article (doi:10.1186/s13071-016-1716-x) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

Transcriptomic analysis of mouse liver reveals a potential hepato-enteric pathogenic mechanism in acute Toxoplasma gondii infection

Elsheikha

et al. 2016

Parasites Vectors

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“…Next, the parasites were stained with Trypan blue. Viable tachyzoites (clear cytoplasm and negative trypan blue staining) and unviable parasites (dark cytoplasm and positive trypan blue staining) were counted under an optical microscope (Castanheira et al, 2015). Tachyzoites in microtubes treated with only medium were considered the control.…”

Section: Methodsmentioning

confidence: 99%

Enrofloxacin and Toltrazuril Are Able to Reduce Toxoplasma gondii Growth in Human BeWo Trophoblastic Cells and Villous Explants from Human Third Trimester Pregnancy

Silva

Gomes

Franco

et al. 2017

Front. Cell. Infect. Microbiol.

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Classical treatment for congenital toxoplasmosis is based on combination of sulfadiazine and pyrimethamine plus folinic acid. Due to teratogenic effects and bone marrow suppression caused by pyrimethamine, the establishment of new therapeutic strategies is indispensable to minimize the side effects and improve the control of infection. Previous studies demonstrated that enrofloxacin and toltrazuril reduced the incidence of Neospora caninum and Toxoplasma gondii infection. The aim of the present study was to evaluate the efficacy of enrofloxacin and toltrazuril in the control of T. gondii infection in human trophoblast cells (BeWo line) and in human villous explants from the third trimester. BeWo cells and villous were treated with several concentrations of enrofloxacin, toltrazuril, sulfadiazine, pyrimethamine, or combination of sulfadiazine+pyrimethamine, and the cellular or tissue viability was verified. Next, BeWo cells were infected by T. gondii (2F1 clone or the ME49 strain), whereas villous samples were only infected by the 2F1 clone. Then, infected cells and villous were treated with all antibiotics and the T. gondii intracellular proliferation as well as the cytokine production were analyzed. Finally, we evaluated the direct effect of enrofloxacin and toltrazuril in tachyzoites to verify possible changes in parasite structure. Enrofloxacin and toltrazuril did not decrease the viability of cells and villous in lower concentrations. Both drugs were able to significantly reduce the parasite intracellular proliferation in BeWo cells and villous explants when compared to untreated conditions. Regardless of the T. gondii strain, BeWo cells infected and treated with enrofloxacin or toltrazuril induced high levels of IL-6 and MIF. In villous explants, enrofloxacin induced high MIF production. Finally, the drugs increased the number of unviable parasites and triggered damage to tachyzoite structure. Taken together, it can be concluded that enrofloxacin and toltrazuril are able to control T. gondii infection in BeWo cells and villous explants, probably by a direct action on the host cells and parasites, which leads to modifications of cytokine release and tachyzoite structure.

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“…BpLec reduced the adhesion and replication of T. gondii tachyzoite in vitro and increased the production of IL‐6 and macrophage migration inhibitory factor by infected HeLa cells previously treated with BpLec (Castanheira et al . ).…”

Section: Antimicrobial Lectinsmentioning

confidence: 97%

Lectins as antimicrobial agents

et al. 2018

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Summary The resistance of micro‐organisms to antimicrobial agents has been a challenge to treat animal and human infections, and for environmental control. Lectins are natural proteins and some are potent antimicrobials through binding to carbohydrates on microbial surfaces. Oligomerization state of lectins can influence their biological activity and maximum binding capacity; the association among lectin polypeptide chains can alter the carbohydrate–lectin binding dissociation rate constants. Antimicrobial mechanisms of lectins include the pore formation ability, followed by changes in the cell permeability and latter, indicates interactions with the bacterial cell wall components. In addition, the antifungal activity of lectins is associated with the chitin‐binding property, resulting in the disintegration of the cell wall or the arrest of de novo synthesis from the cell wall during fungal development or division. Quorum sensing is a cell‐to‐cell communication process that allows interspecies and interkingdom signalling which coordinate virulence genes; antiquorum‐sensing therapies are described for animal and plant lectins. This review article, among other approaches, evaluates lectins as antimicrobials.

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Insights into anti-parasitism induced by a C-type lectin from Bothrops pauloensis venom on Toxoplasma gondii

Cited by 30 publications

References 44 publications

Transcriptomic analysis of mouse liver reveals a potential hepato-enteric pathogenic mechanism in acute Toxoplasma gondii infection

Transcriptomic analysis of mouse liver reveals a potential hepato-enteric pathogenic mechanism in acute Toxoplasma gondii infection

Enrofloxacin and Toltrazuril Are Able to Reduce Toxoplasma gondii Growth in Human BeWo Trophoblastic Cells and Villous Explants from Human Third Trimester Pregnancy

Lectins as antimicrobial agents

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