Elementos do sistema nervoso central parasitados pelo Trypanosoma cruzi

Villela, Eurico

doi:10.1590/s0074-02761932000100004

Cited by 18 publications

(5 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Therefore, susceptibility of astrocytes to T. cruzi infection in vitro is preserved in different mouse genetic backgrounds and among species. In Chagas disease patients and experimental models, astrocytes are preferred targets for T. cruzi invasion and proliferation in the CNS, regardless of the host species and parasite strain [ 21 , 26 , 29 , 44 ]. Thus, the experimental models proposed here are appropriate to test our hypotheses.…”

Section: Discussionmentioning

confidence: 99%

Priming astrocytes with TNF enhances their susceptibility to Trypanosoma cruzi infection and creates a self-sustaining inflammatory milieu

Silva

Gibaldi

et al. 2017

J Neuroinflammation

View full text Add to dashboard Cite

Background: In conditions of immunosuppression, the central nervous sty 5ystem (CNS) is the main target tissue for the reactivation of infection by Trypanosoma cruzi, the causative agent of Chagas disease. In experimental T. cruzi infection, interferon gamma (IFNγ) + microglial cells surround astrocytes harboring amastigote parasites. In vitro, IFNγ fuels astrocyte infection by T. cruzi, and IFNγ-stimulated infected astrocytes are implicated as potential sources of tumor necrosis factor (TNF). Pro-inflammatory cytokines trigger behavioral alterations. In T. cruzi-infected mice, administration of anti-TNF antibody hampers depressive-like behavior. Herein, we investigated the effects of TNF on astrocyte susceptibility to T. cruzi infection and the regulation of cytokine production. Methods: Primary astrocyte cultures of neonatal C57BL/6 and C3H/He mice and the human U-87 MG astrocyte lineage were infected with the Colombian T. cruzi strain. Cytokine production, particularly TNF, and TNF receptor 1 (TNFR1/p55) expression were analyzed. Recombinant cytokines (rIFNγ and rTNF), the anti-TNF antibody infliximab, and the TNFR1 modulator pentoxifylline were used to assess the in vitro effects of TNF on astrocyte susceptibility to T. cruzi infection. To investigate the role of TNF on CNS colonization by T. cruzi, infected mice were submitted to anti-TNF therapy. Results: rTNF priming of mouse and human astrocytes enhanced parasite/astrocyte interaction (i.e., the percentage of astrocytes invaded by trypomastigote parasites and the number of intracellular parasite forms/astrocyte). Furthermore, T. cruzi infection drove astrocytes to a pro-inflammatory profile with TNF and interleukin-6 production, which was amplified by rTNF treatment. Adding rTNF prior to infection fueled parasite growth and trypomastigote egression, in parallel with increased TNFR1 expression. Importantly, pentoxifylline inhibited the TNF-induced increase in astrocyte susceptibility to T. cruzi invasion. In T. cruzi-infected mice, anti-TNF therapy reduced the number of amastigote nests in the brain.

show abstract

Section: Discussionmentioning

confidence: 99%

Priming astrocytes with TNF enhances their susceptibility to Trypanosoma cruzi infection and creates a self-sustaining inflammatory milieu

Silva

Gibaldi

et al. 2017

J Neuroinflammation

View full text Add to dashboard Cite

show abstract

“…In Chagasic megacolon, the alteration of the number of enteric glial cells, as well as glial activation markers, suggests that these cells participate in the inflammatory process and in the subsequent neuronal damage or protection [15,21]. Actually, glial cells have been shown to be parasitized by T. cruzi in both the central nervous system (CNS) and the enteric nervous system (ENS) [7,[22][23][24][25].…”

Section: An Immunological Overview Of Chagasic Megacolonmentioning

confidence: 99%

Biomarkers and Their Possible Functions in the Intestinal Microenvironment of Chagasic Megacolon: An Overview of the (Neuro)inflammatory Process

Neto

Braga

Costa

et al. 2021

Journal of Immunology Research

View full text Add to dashboard Cite

The association between inflammatory processes and intestinal neuronal destruction during the progression of Chagasic megacolon is well established. However, many other components play essential roles, both in the long-term progression and control of the clinical status of patients infected with Trypanosoma cruzi. Components such as neuronal subpopulations, enteric glial cells, mast cells and their proteases, and homeostasis-related proteins from several organic systems (serotonin and galectins) are differentially involved in the progression of Chagasic megacolon. This review is aimed at revealing the characteristics of the intestinal microenvironment found in Chagasic megacolon by using different types of already used biomarkers. Information regarding these components may provide new therapeutic alternatives and improve the understanding of the association between T. cruzi infection and immune, endocrine, and neurological system changes.

show abstract

“…Foi Gaspar Vianna 72 o primeiro a demonstrar o parasitismo das células gliais, achado corroborado por outros pesquisadores, esclarecendo-se que não só a astroglia é parasitada, mas, também e particularmente, a microglia 70 -79 > 80 . 81 .…”

Section: G7unclassified

“…79 , presença das leishmânias no interior das células da neuroglia (astroglia e microglia) 80 . 81 e, mais raramente, nas células neuronals 81 , fenômenos degenerativos dos neurônios adjacentes aos granulomas lñ > 79 , das células de Purkinje, das células piramidais e, menos acentuadamente, das células ganglionares da medula 12 . 80 , infiltrados inflamatorios meníngeos e lesões vasculares adventiciais e da íntima 14 .…”

Section: G7unclassified

Aspectos neurológicos da doença de chagas: sistema nervoso central

Forjaz

1967

Arq. Neuro-Psiquiatr.

View full text Add to dashboard Cite

A leitura dos trabalhos de Carlos Chagas sobre a tripanosomíase e a meditação sobre afirmações quanto aos acometimentos do sistema nervoso central (SNC) nessa moléstia, suscita uma série de questões que os esforços de vários pesquisadores ainda não conseguiram dirimir.Aos 30 anos de idade, Carlos Chagas, médico sanitarista, nunca havia sido neurologista militante, nem tampouco, neuropatologista. A pobreza dos recursos da Neurologia naquela época, sobretudo em pleno sertão, teria feito qualquer especialista de nossos dias desanimar antes do início de qualquer pesquisa, mesmo que a grandeza dos resultados lhe fosse mágicamente revelada por antecipação. Daí o significado do trabalho deste sábio brasileiro, cuja argúcia, associada a sólida cultura e fé inabalável nas próprias convicções, sustentaram a chama criadora, na qual moldou sua obra científica.Entretanto, por muito que se admire o grande sábio e sua obra, no campo especial da Neurologia certas questões permanecem abertas: as manifestações sintomáticas que formam síndromes de Little e da diplegia cerebral espástica seriam realmente formas crônicas, evolutivas, da moléstia, como Chagas apontou, ou seriam simples seqüelas, "patias", ou mesmo manifestações de outras moléstias superpostas à tripanosomíase, com incidên-cia acidentalmente acrescida nas populações flageladas em que Chagas descobriu seus primeiros doentes? Quais, então, as verdadeiras formas crônicas da moléstia conseqüentes às formas agudas tão bem configuradas? Como diagnosticá-las comprovadamente? Foi com o espírito voltado para tais incógnitas que reestudamos as publicações relacionadas com este tema. Os comentários subseqüentes serão feitos com o objetivo de procurar respondê-las.O acometimento do SNC na doença de Chagas resulta de dois mecanismos diversos: 1) a penetração do tripanosoma no eixo encefalomedular; 2) os acidentes embólicos na cardiopatia crônica. Constituem estes últimos antes uma complicação neurológica que propriamente o substrato de uma forma clínica da doença. A designação de forma nervosa, de autoria do próprio Chagas 18 . 21 , tem sido habitualmente aplicada apenas às lesões e manifestações sintomáticas que resultam da invasão do SNC pelo T. cruzi.

show abstract

Elementos do sistema nervoso central parasitados pelo Trypanosoma cruzi

Cited by 18 publications

References 0 publications

Priming astrocytes with TNF enhances their susceptibility to Trypanosoma cruzi infection and creates a self-sustaining inflammatory milieu

Priming astrocytes with TNF enhances their susceptibility to Trypanosoma cruzi infection and creates a self-sustaining inflammatory milieu

Biomarkers and Their Possible Functions in the Intestinal Microenvironment of Chagasic Megacolon: An Overview of the (Neuro)inflammatory Process

Aspectos neurológicos da doença de chagas: sistema nervoso central

Contact Info

Product

Resources

About