In vivo macrophage function in experimental infection with Trypanosoma cruzi subpopulations

Acta Tropica ◽  
1993 ◽  
Vol 55 (3) ◽  
pp. 171-180 ◽  
Author(s):  
Ana M. Celentano ◽  
Stella M. González Cappa
Keyword(s):  
Trypanosoma Cruzi ◽  
Experimental Infection ◽  
Macrophage Function

Effects of Highly Diluted Drugs on Experimental Infection with Trypanosoma cruzi In Vivo: Systematic Review

2020 ◽  
Vol 26 (10) ◽  
pp. 866-883
Author(s):  
Daniela Cristina Grégio d'Arce Mota ◽  
Érika Cristina Ferreira ◽  
Fabiana Nabarro Ferraz ◽  
Maria Vitória Felipe de Souza ◽  
Bruna Lauton Simões ◽  
...  
Keyword(s):  
Systematic Review ◽  
Trypanosoma Cruzi ◽  
Experimental Infection

scholarly journals Interleukin-9 in Immunopathology of Trypanosoma cruzi Experimental Infection

2021 ◽  
Vol 11 ◽  
Author(s):  
Nadjania Saraiva de Lira Silva ◽  
Cristina Mary Orikaza ◽  
Fabiana Rodrigues de Santana ◽  
Luana Aguiar dos Santos ◽  
Bruno Ramos Salu ◽  
...  
Keyword(s):  
Trypanosoma Cruzi ◽  
Chagas Disease ◽  
Experimental Infection ◽  
Cardiac Fibrosis ◽  
Tissue Injury ◽  
Chronic Phase ◽  
Protective Role

Chagas’ disease is a parasitosis caused by Trypanosoma cruzi, which affects approximately 8 million people worldwide. The balance between pro- and anti-inflammatory cytokines produced during immunological responses contributes to disease prognosis and progression. Parasite tissue persistence can induce chronic inflammatory stimuli, which can cause long-term tissue injury and fibrosis. Chronic Chagas’ patients exhibit increased levels of interleukin (IL)-9, an important cytokine in the regulation of inflammatory and fibrogenic processes. Data on the role of IL-9 in other pathologies are sometimes contradictory, and few studies have explored this cytokine’s influence in Chagas’ disease pathology. Hence, the aim of this study was to evaluate the role of IL-9 in the progression of T. cruzi infection in vivo and in vitro. In vitro infection demonstrated that IL-9 reduced the number of infected cells and decreased the multiplication of intracellular amastigotes in both C2C12 myoblasts and bone marrow-derived macrophages. In myoblasts, the increased production of nitric oxide (NO) was essential for reduced parasite multiplication, whereas macrophage responses resulted in increased IL-6 and reduced TGF-β levels, indicating that parasite growth restriction mechanisms induced by IL-9 were cell-type specific. Experimental infection of BALB/c mice with T. cruzi trypomastigotes of the Y strain implicated a major role of IL-9 during the chronic phase, as increased Th9 and Tc9 cells were detected among splenocytes; higher levels of IL-9 in these cell populations and increased cardiac IL-9 levels were detected compared to those of uninfected mice. Moreover, rIL9 treatment decreased serum IL-12, IL-6, and IL-10 levels and cardiac TNF-α levels, possibly attempting to control the inflammatory response. IL-9 neutralization increased cardiac fibrosis, synthesis of collagens I and III, and mastocyte recruitment in BALB/c heart tissue during the chronic phase. In conclusion, our data showed that IL-9 reduced the invasion and multiplication of T. cruzi in vitro, in both myoblasts and macrophages, favoring disease control through cell-specific mechanisms. In vivo, IL-9 was elevated during experimental chronic infection in BALB/c mice, and this cytokine played a protective role in the immunopathological response during this phase by controlling cardiac fibrosis and proinflammatory cytokine production.

scholarly journals Evaluation of effects of inert vehicles proceeding from homeopathic preparation in mice’s experimental infection by Trypanosoma cruzi

2021 ◽  
Vol 13 (47) ◽  
pp. 108-110
Author(s):  
Angela Rigo Portocarrero ◽  
Patrícia Flora Sandri ◽  
Franciele Karina Da Veiga ◽  
Larissa Ciupa ◽  
Fabiana Nabarro Ferraz ◽  
...  
Keyword(s):  
Life Expectancy ◽  
Trypanosoma Cruzi ◽  
Experimental Infection ◽  
Alcoholic Solution ◽  
In Vivo Studies ◽  
Control Group ◽  
Patent Period ◽  
Increasing Trend ◽  
Homeopathic Preparation

Background: In experiments with homeopathic medicines is important to test the inert vehicle from succussed preparations for the treatment control. Aim: To evaluate the effect of hydro-alcoholic solutions 1cH, 6cH and 30cH in mice’s experimental infection with Trypanosoma cruzi. Methodology: In a blind, randomized, controlled test, two independent experiments with 34 and 51 swiss male mice, 8 weeks old, kept in cages micro acclimated, infected with 1400 blood trypomastigotes of the Y strain of T. cruzi (via IP), were divided: IC-untreated control; G1cH-received hydro-alcoholic solution dynamized 1cH; G6cH-received hydro-alcoholic solution dynamized 6cH and G30cH-received hydro-alcoholic solution dynamized 30cH. The solutions were prepared according to Brazilian Homeophatic Pharmacopoeia1 with alcohol 70 ° GL. Final preparations (1cH, 6cH and 30cH) were manipulated with water (Sigma-SP-Brazil). The treatment was offered diluted with water (1/100mL) ad libitum 48 hours before infection, available for 16h. After infection, the animals were treated 56h/56h for 16h until the 9th day of infection. The parasitological parameters were analyzed: Curve of Parasitemia, Total Parasitemia (TP), Peak Maximum of Parasites (PMP), Pre-Patent Period (PPP), Patent Period (PP) and Survival. The experiment was approved by the UEM’s Ethical Committee. Results: G1cH showed a higher survival (p=0.044) with a life expectancy of 2.58 times larger than the control group (Figure 1.A), as well as lower TP (p=0.002) and PMP (p = 0.018). PPP and PP showed no statistical difference, although in G1cH1 it was observed an increasing trend of PPP (p=0.065). These results are related to host’s benefit. The G6cH group presented a longer survival (p=0,045), with a life expectancy 1.94 times larger than the control group (Figure 1.B). Although no difference to TP, PMP, PP and PPP has been observed, the alcohol 6cH performed protecting animals against infection. The G30cH displayed an increasing trend of PMP (p=0.066) compared to the control group. Effects of inert vehicle succussed have been reported in studies in vitro2. However, no effects had been reported in vivo studies yet2,3. The hydro-alcoholic solution 7% 13CH, tested under the same conditions and animal model, did not change the natural evolution of the infection2. Conclusion: The hydro-alcoholic solutions 1cH and 6cH altered the course of experimental infection by T. cruzi, reducing the parasitemia and/or increasing the survival time, and can not be considered as inert vehicle in the high diluted compounds preparation.

Unusual dimeric flavonoids from Arrabidaea brachypoda with very significant in vitro and in vivo anti-Trypanosoma cruzi activity

Planta Medica ◽  
2014 ◽  
Vol 80 (16) ◽  
Author(s):  
C Quitino-da-Rocha ◽  
E Ferreira-Queiroz ◽  
C Santana-Meira ◽  
DR Magalhães-Moreira ◽  
M Botelho-Pereira-Soares ◽  
...  
Keyword(s):  
Trypanosoma Cruzi

scholarly journals Neurotrophin Receptor TrkC Is an Entry Receptor for Trypanosoma cruzi in Neural, Glial, and Epithelial Cells

2011 ◽  
Vol 79 (10) ◽  
pp. 4081-4087 ◽  
Author(s):  
Craig Weinkauf ◽  
Ryan Salvador ◽  
Mercio PereiraPerrin
Keyword(s):  
Trypanosoma Cruzi ◽  
Chagas Disease ◽  
Mammalian Cells ◽  
Chinese Hamster ◽  
Neuronal Cell ◽  
Host Cells ◽  
Neurotrophin Receptor ◽  
Content Type

ABSTRACTTrypanosoma cruzi, the agent of Chagas' disease, infects a variety of mammalian cells in a process that includes multiple cycles of intracellular division and differentiation starting with host receptor recognition by a parasite ligand(s). Earlier work in our laboratory showed that the neurotrophin-3 (NT-3) receptor TrkC is activated byT. cruzisurfacetrans-sialidase, also known as parasite-derived neurotrophic factor (PDNF). However, it has remained unclear whether TrkC is used byT. cruzito enter host cells. Here, we show that a neuronal cell line (PC12-NNR5) relatively resistant toT. cruzibecame highly susceptible to infection when overexpressing human TrkC but not human TrkB. Furthermore,trkCtransfection conferred an ∼3.0-fold intracellular growth advantage. Sialylation-deficient Chinese hamster ovarian (CHO) epithelial cell lines Lec1 and Lec2 also became much more permissive toT. cruziafter transfection with thetrkCgene. Additionally, NT-3 specifically blockedT. cruziinfection of the TrkC-NNR5 transfectants and of naturally permissive TrkC-bearing Schwann cells and astrocytes, as did recombinant PDNF. Two specific inhibitors of Trk autophosphorylation (K252a and AG879) and inhibitors of Trk-induced MAPK/Erk (U0126) and Akt kinase (LY294002) signaling, but not an inhibitor of insulin-like growth factor 1 receptor, abrogated TrkC-mediated cell invasion. Antibody to TrkC blockedT. cruziinfection of the TrkC-NNR5 transfectants and of cells that naturally express TrkC. The TrkC antibody also significantly and specifically reduced cutaneous infection in a mouse model of acute Chagas' disease. TrkC is ubiquitously expressed in the peripheral and central nervous systems, and in nonneural cells infected byT. cruzi, including cardiac and gastrointestinal muscle cells. Thus, TrkC is implicated as a functional PDNF receptor in cell entry, independently of sialic acid recognition, mediating broadT. cruziinfection bothin vitroandin vivo.

scholarly journals Benznidazole Treatment following Acute Trypanosoma cruzi Infection Triggers CD8+ T-Cell Expansion and Promotes Resistance to Reinfection

2002 ◽  
Vol 46 (12) ◽  
pp. 3790-3796 ◽  
Author(s):  
Bianca Perdigão Olivieri ◽  
Vinícius Cotta-de-Almeida ◽  
Tania Araújo-Jorge
Keyword(s):  
T Lymphocytes ◽  
Trypanosoma Cruzi ◽  
Immune Regulation ◽  
Immune Dysregulation ◽  
Direct Role ◽  
Parasite Replication ◽  
The Impact ◽  
Shed Light ◽  
Cruzi Infection

ABSTRACT Many studies have shed light on the mechanisms underlying both immunoprotection and immune dysregulation arising after Trypanosoma cruzi infection. However, little is known about the impact of benznidazole (N-benzyl-2-nitroimidazole acetamide), the drug available for clinical treatment of the infection, on the immune system in the infected host. In the present study we investigated the effect of benznidazole therapy on the lymphoid compartment during the course of experimental T. cruzi infection. Although amelioration of a variety of clinical and parasitological signs was observed in treated mice, amelioration of splenocyte expansion was not detected. Interestingly, this sustained splenomegaly observed in benznidazole-treated mice showed a preferential expansion of CD8+ T lymphocytes. Moreover, although benznidazole treatment blocked the expansion of recently activated CD4+ and CD8+ T cells seen in infected hosts, benznidazole treatment led to a selective expansion of effector and memory CD8+ T lymphocytes in association with a lower rate of apoptosis. In addition, the surviving treated animals were protected from reinfection. Together, these data suggest that, in addition to its well-known direct role in blocking parasite replication in vivo, benznidazole appears to directly affect immune regulation in T. cruzi-infected hosts.

scholarly journals Transcription of Candidate Virulence Genes ofHaemophilus ducreyi during Infection of Human Volunteers

2001 ◽  
Vol 69 (3) ◽  
pp. 1483-1487 ◽  
Author(s):  
Robert E. Throm ◽  
Stanley M. Spinola
Keyword(s):  
Experimental Infection ◽  
Virulence Genes ◽  
Human Model ◽  
Specific Gene ◽  
Gene Products ◽  
Virulence Determinants ◽  
Reverse Transcription Pcr ◽  
Human Volunteers

ABSTRACT Haemophilus ducreyi expresses several putative virulence factors in vitro. Isogenic mutant-to-parent comparisons have been performed in a human model of experimental infection to examine whether specific gene products are involved in pathogenesis. Several mutants (momp, ftpA, losB, lst, cdtC, and hhdB) were as virulent as the parent in the human model, suggesting that their gene products did not play a major role in pustule formation. However, we could not exclude the possibility that the gene of interest was not expressed during the initial stages of infection. Biopsies of pustules obtained from volunteers infected with H. ducreyiwere subjected to reverse transcription-PCR. Transcripts corresponding to momp, ftpA, losB, lst, cdtB, and hhdA were expressed in vivo. In addition, transcripts for other putative virulence determinants such as ompA2, tdhA, lspA1, andlspA2 were detected in the biopsies. These results indicate that although several candidate virulence determinants are expressed during experimental infection, they do not have a major role in the initial stages of pathogenesis.

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