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1.
Alejandro O Luquetti Suelene Brito do Nascimento Tavares Liliane da Rocha Siriano Rozangela Amaral de Oliveira Dayse Elizabeth Campos Cicilio Alves de Morais Enio Chaves de Oliveira 《Memórias do Instituto Oswaldo Cruz》2015,110(3):369-376
Transmission of Trypanosoma cruzi during pregnancy is estimated to
occur in less than 20% of infected mothers; however, the etiopathogenesis is not
completely understood. The Centre for Studies on Chagas Disease provides confirmation
of T. cruzi infection for individuals living in central Brazil.
In this retrospective hospital-based study, all requests for diagnosis of T.
cruzi infection in individuals less than 21 years old from 1994-2014 were
searched. We end with 1,211 individuals and their respective infected mothers.
Congenital transmission of infection was confirmed in 24 individuals (2%) in central
Brazil, an area where the main T. cruzi lineage circulating in
humans is TcII. This low prevalence of congenital Chagas disease is discussed in
relation to recent findings in the south region of Brazil, where TcV is the main
lineage and congenital transmission has a higher prevalence (approximately 5%),
similar to frequencies reported in Argentina, Paraguay and Bolivia. This is the first
report to show geographical differences in the rates of congenital transmission
of T. cruzi and the relationship between the prevalence of
congenital transmission and the type of Tc prevalent in each region. 相似文献
2.
Camila Megale de Almeida-Leite Isabel Cristina Costa Silva Lúcia Maria da Cunha Galv?o Rosa Maria Esteves Arantes 《Memórias do Instituto Oswaldo Cruz》2014,109(4):459-465
Nitric oxide (NO) participates in neuronal lesions in the digestive form of Chagas
disease and the proximity of parasitised glial cells and neurons in damaged myenteric
ganglia is a frequent finding. Glial cells have crucial roles in many
neuropathological situations and are potential sources of NO. Here, we investigate
peripheral glial cell response to Trypanosoma cruzi infection to
clarify the role of these cells in the neuronal lesion pathogenesis of Chagas
disease. We used primary glial cell cultures from superior cervical ganglion to
investigate cell activation and NO production after T. cruzi
infection or lipopolysaccharide (LPS) exposure in comparison to peritoneal
macrophages. T. cruzi infection was greater in glial cells, despite
similar levels of NO production in both cell types. Glial cells responded similarly
to T. cruzi and LPS, but were less responsive to LPS than
macrophages were. Our observations contribute to the understanding of Chagas disease
pathogenesis, as based on the high susceptibility of autonomic glial cells to
T. cruzi infection with subsequent NO production. Moreover, our findings
will facilitate future research into the immune responses and activation mechanisms
of peripheral glial cells, which are important for understanding the paradoxical
responses of this cell type in neuronal lesions and neuroprotection. 相似文献
3.
María Cecilia Albareda Susana Adriana Laucella 《Memórias do Instituto Oswaldo Cruz》2015,110(3):414-421
The aim of this review is to describe the contributions of the knowledge of T-cell
responses to the understanding of the physiopathology and the responsiveness to
etiological treatment during the chronic phase of Chagas disease.
T-helper (Th)1 and interleukin (IL)-10 Trypanosoma
cruzi-specific T-cells have been linked to the asymptomatic phase or to
severe clinical forms of the disease, respectively or vice versa,
depending on the T. cruzi antigen source, the patient’s location and
the performed immunological assays. Parasite-specific T-cell responses are modulated
after benznidazole (BZ) treatment in chronically T. cruzi-infected
subjects in association with a significant decrease in T.
cruzi-specific antibodies. Accumulating evidence has indicated that
treatment efficacy during experimental infection with T. cruzi
results from the combined action of BZ and the activation of appropriate
immune responses in the host. However, strong support of this interaction in
T. cruzi-infected humans remains lacking. Overall, the quality of T-cell
responses might be a key factor in not only disease evolution, but also chemotherapy
responsiveness. Immunological parameters are potential indicators of treatment
response regardless of achievement of cure. Providing tools to monitor and provide
early predictions of treatment success will allow the development of new therapeutic
options. 相似文献
4.
Rana Nagarkatti Fernanda Fortes de Araujo Charu Gupta Alain Debrabant 《PLoS neglected tropical diseases》2014,8(1)
Chagas disease affects about 5 million people across the world. The etiological agent, the intracellular parasite Trypanosoma cruzi (T. cruzi), can be diagnosed using microscopy, serology or PCR based assays. However, each of these methods has their limitations regarding sensitivity and specificity, and thus to complement these existing diagnostic methods, alternate assays need to be developed. It is well documented that several parasite proteins called T. cruzi Excreted Secreted Antigens (TESA), are released into the blood of an infected host. These circulating parasite antigens could thus be used as highly specific biomarkers of T. cruzi infection. In this study, we have demonstrated that, using a SELEx based approach, parasite specific ligands called aptamers, can be used to detect TESA in the plasma of T. cruzi infected mice. An Enzyme Linked Aptamer (ELA) assay, similar to ELISA, was developed using biotinylated aptamers to demonstrate that these RNA ligands could interact with parasite targets. Aptamer L44 (Apt-L44) showed significant and specific binding to TESA as well as T. cruzi trypomastigote extract and not to host proteins or proteins of Leishmania donovani, a related trypanosomatid parasite. Our result also demonstrated that the target of Apt-L44 is conserved in three different strains of T. cruzi. In mice infected with T. cruzi, Apt-L44 demonstrated a significantly higher level of binding compared to non-infected mice suggesting that it could detect a biomarker of T. cruzi infection. Additionally, Apt-L44 could detect these circulating biomarkers in both the acute phase, from 7 to 28 days post infection, and in the chronic phase, from 55 to 230 days post infection. Our results show that Apt-L44 could thus be used in a qualitative ELA assay to detect biomarkers of Chagas disease. 相似文献
5.
Trypanosoma cruzi: effect of the infection on the 20S proteasome in non-immune cells 总被引:1,自引:0,他引:1
Human infection with the protozoan Trypanosoma cruzi leads to Chagas disease. After 10-20 years of the normal acute phase, this disease develops to a chronic phase characterized mainly by dilated congestive cardiomyopathy. The mechanisms involved in the chronic phase are poorly understood, and it has been suggested that the parasite evades immune surveillance by down regulating the MHC class I antigen processing pathway. Here we analyzed whether composition or expression of the 20S proteasome, the major proteinase responsible for the generation of MHC class I ligands, were altered upon infection of HeLa cells by T. cruzi. Two-dimensional gel electrophoresis and RT-PCR experiments comparing non-infected and infected cells did not show differences between the composition of 20S proteasome or expression of its subunits. However, the proteasome’s trypsin- and chymotrypsin-like activities were 2.5 and 3.6 times higher in infected cells than in non-infected cells. Our results suggest that in vitroT. cruzi infection of human or rat cells do not alter the expression of 20S proteasomal subunits or particle composition, and fails to induce the formation of immunoproteasome. However, a significant increase in the trypsin- and chymotrypsin-like activities of the host proteasome was observed. 相似文献
6.
Antonio Gigliotti Rothfuchs Ester Roffê Amanda Gibson Allen W. Cheever R. Alan B. Ezekowitz Kazue Takahashi Mario Steindel Alan Sher André Báfica 《PloS one》2012,7(11)
Mannose-binding lectin (MBL) is a humoral pattern-recognition molecule important for host defense. Although recent genetic studies suggest an involvement of MBL/MASP2-associated pathways in Chagas’ disease, it is currently unknown whether MBL plays a role in host resistance to the intracellular protozoan Trypanosoma cruzi, the causative agent of Chagas’ disease. In this study we employed MBL−/− mice to assess the role of MBL in resistance to experimental infection with T. cruzi. T. cruzi infection enhanced tissue expression of MBL both at the mRNA and protein level. Similarly, symptomatic acute Chagas’ disease patients displayed increased serum concentrations of MBL compared to patients with indeterminate, asymptomatic forms of the disease. Furthermore, increased parasite loads in the blood and/or tissue were observed in MBL−/− mice compared to WT controls. This was associated with reduced systemic levels of IL-12/23p40 in MBL−/− mice. Importantly, MBL−/− mice infected with a cardiotropic strain of T. cruzi displayed increased myocarditis and cardiac fibrosis compared to WT controls. The latter was accompanied by elevated hydroxyproline content and mRNA levels of collagen-1 and -6 in the heart. These observations point to a previously unappreciated role for MBL in regulating host resistance and cardiac inflammation during infection with a major human pathogen. 相似文献
7.
Nagajyothi F Weiss LM Silver DL Desruisseaux MS Scherer PE Herz J Tanowitz HB 《PLoS neglected tropical diseases》2011,5(2):e953
Background
Trypanosoma cruzi, an intracellular protozoan parasite that infects humans and other mammalian hosts, is the etiologic agent in Chagas disease. This parasite can invade a wide variety of mammalian cells. The mechanism(s) by which T. cruzi invades its host cell is not completely understood. The activation of many signaling receptors during invasion has been reported; however, the exact mechanism by which parasites cross the host cell membrane barrier and trigger fusion of the parasitophorous vacuole with lysosomes is not understood.Methodology/Principal Findings
In order to explore the role of the Low Density Lipoprotein receptor (LDLr) in T. cruzi invasion, we evaluated LDLr parasite interactions using immunoblot and immunofluorescence (IFA) techniques. These experiments demonstrated that T. cruzi infection increases LDLr levels in infected host cells, inhibition or disruption of LDLr reduces parasite load in infected cells, T. cruzi directly binds recombinant LDLr, and LDLr-dependent T. cruzi invasion requires PIP2/3. qPCR analysis demonstrated a massive increase in LDLr mRNA (8000 fold) in the heart of T. cruzi infected mice, which is observed as early as 15 days after infection. IFA shows a co-localization of both LDL and LDLr with parasites in infected heart.Conclusions/Significance
These data highlight, for the first time, that LDLr is involved in host cell invasion by this parasite and the subsequent fusion of the parasitophorous vacuole with the host cell lysosomal compartment. The model suggested by this study unifies previous models of host cell invasion for this pathogenic protozoon. Overall, these data indicate that T. cruzi targets LDLr and its family members during invasion. Binding to LDL likely facilitates parasite entry into host cells. The observations in this report suggest that therapeutic strategies based on the interaction of T. cruzi and the LDLr pathway should be pursued as possible targets to modify the pathogenesis of disease following infection. 相似文献8.
9.
Cristiane Varella Lisboa Rafael Veríssimo Monteiro Andreia Fonseca Martins Samantha Cristina das Chagas Xavier Valdirene dos Santos Lima Ana Maria Jansen 《Memórias do Instituto Oswaldo Cruz》2015,110(3):394-402
Here, we present a review of the dataset resulting from the 11-years follow-up of
Trypanosoma cruzi infection in free-ranging populations of
Leontopithecus rosalia (golden lion tamarin) and
Leontopithecus chrysomelas (golden-headed lion tamarin) from
distinct forest fragments in Atlantic Coastal Rainforest. Additionally, we present
new data regarding T. cruzi infection of small mammals (rodents and
marsupials) that live in the same areas as golden lion tamarins and characterisation
at discrete typing unit (DTU) level of 77 of these isolates. DTU TcII was found to
exclusively infect primates, while TcI infected Didelphis aurita and
lion tamarins. The majority of T. cruzi isolates derived from
L. rosalia were shown to be TcII (33 out 42) Nine T.
cruzi isolates displayed a TcI profile. Golden-headed lion tamarins
demonstrated to be excellent reservoirs of TcII, as 24 of 26 T.
cruzi isolates exhibited the TcII profile. We concluded the following:
(i) the transmission cycle of T. cruzi in a same host species and
forest fragment is modified over time, (ii) the infectivity competence of the golden
lion tamarin population fluctuates in waves that peak every other year and (iii) both
golden and golden-headed lion tamarins are able to maintain long-lasting infections
by TcII and TcI. 相似文献
10.
Rodrigues CM Valadares HM Francisco AF Arantes JM Campos CF Teixeira-Carvalho A Martins-Filho OA Araujo MS Arantes RM Chiari E Franco GR Machado CR Pena SD Faria AM Macedo AM 《PLoS neglected tropical diseases》2010,4(10):e846
A century after the discovery of Trypanosoma cruzi in a child living in Lassance, Minas Gerais, Brazil in 1909, many uncertainties remain with respect to factors determining the pathogenesis of Chagas disease (CD). Herein, we simultaneously investigate the contribution of both host and parasite factors during acute phase of infection in BALB/c mice infected with the JG and/or CL Brener T. cruzi strains. JG single infected mice presented reduced parasitemia and heart parasitism, no mortality, levels of pro-inflammatory mediators (TNF-α, CCL2, IL-6 and IFN-γ) similar to those found among naïve animals and no clinical manifestations of disease. On the other hand, CL Brener single infected mice presented higher parasitemia and heart parasitism, as well as an increased systemic release of pro-inflammatory mediators and higher mortality probably due to a toxic shock-like systemic inflammatory response. Interestingly, coinfection with JG and CL Brener strains resulted in intermediate parasitemia, heart parasitism and mortality. This was accompanied by an increase in the systemic release of IL-10 with a parallel increase in the number of MAC-3+ and CD4+ T spleen cells expressing IL-10. Therefore, the endogenous production of IL-10 elicited by coinfection seems to be crucial to counterregulate the potentially lethal effects triggered by systemic release of pro-inflammatory mediators induced by CL Brener single infection. In conclusion, our results suggest that the composition of the infecting parasite population plays a role in the host response to T. cruzi in determining the severity of the disease in experimentally infected BALB/c mice. The combination of JG and CL Brener was able to trigger both protective inflammatory immunity and regulatory immune mechanisms that attenuate damage caused by inflammation and disease severity in BALB/c mice. 相似文献
11.
Trypanosoma cruzi infection is a major public health problem in Latin America. The host innate immune system plays a pivotal role in the recognition of T. cruzi infection and the subsequent development of adaptive immunity. In this review, we focus on the TLR-dependent and -independent innate immune responses to T. cruzi. 相似文献
12.
《Microbes and infection / Institut Pasteur》2014,16(9):768-777
Previous studies have demonstrated loss/reduction of dystrophin in cardiomyocytes in both acute and chronic stages of experimental Trypanosoma cruzi (T. cruzi) infection in mice. The mechanisms responsible for dystrophin disruption in the hearts of mice acutely infected with T. cruzi are not completely understood. The present in vivo and in vitro studies were undertaken to evaluate the role of inflammation in dystrophin disruption and its correlation with the high mortality rate during acute infection. C57BL/6 mice were infected with T. cruzi and killed 14, 20 and 26 days post infection (dpi). The intensity of inflammation, cardiac expression of dystrophin, calpain-1, NF-κB, TNF-α, and sarcolemmal permeability were evaluated. Cultured neonatal murine cardiomyocytes were incubated with serum, collected at the peak of cytokine production and free of parasites, from T. cruzi-infected mice and dystrophin, calpain-1, and NF-κB expression analyzed. Dystrophin disruption occurs at the peak of mortality and inflammation and is associated with increased expression of calpain-1, TNF-α, NF-κB, and increased sarcolemmal permeability in the heart of T. cruzi-infected mice at 20 dpi confirmed by in vitro studies. The peak of mortality occurred only when significant loss of dystrophin in the hearts of infected animals occurred, highlighting the correlation between inflammation, dystrophin loss and mortality. 相似文献
13.
Cíntia Júnia Monteiro Suianne Letícia Antunes Mota Lívia de Figueiredo Diniz Maria Terezinha Bahia Karen CM Moraes 《Memórias do Instituto Oswaldo Cruz》2015,110(8):996-1002
Chagas disease, which is caused by the intracellular protozoanTrypanosoma
cruzi, is a serious health problem in Latin America. The heart is one of
the major organs affected by this parasitic infection. The pathogenesis of tissue
remodelling, particularly regarding cardiomyocyte behaviour after parasite infection,
and the molecular mechanisms that occur immediately following parasite entry into
host cells are not yet completely understood. Previous studies have reported that the
establishment of parasitism is connected to the activation of the
phosphatidylinositol-3 kinase (PI3K), which controls important steps in cellular
metabolism by regulating the production of the second messenger
phosphatidylinositol-3,4,5-trisphosphate. Particularly, the tumour suppressor PTEN is
a negative regulator of PI3K signalling. However, mechanistic details of the
modulatory activity of PTEN on Chagas disease have not been elucidated. To address
this question, H9c2 cells were infected with T. cruzi Berenice 62
strain and the expression of a specific set of microRNAs (miRNAs) were investigated.
Our cellular model demonstrated that miRNA-190b is correlated to the decrease of
cellular viability rates by negatively modulating PTEN protein expression in
T. cruzi-infected cells. 相似文献
14.
Ailin Lepletier Vinicius Frias de Carvalho Patricia Machado Rodrigues e Silva Silvina Villar Ana Rosa Pérez Wilson Savino Alexandre Morrot 《PLoS neglected tropical diseases》2013,7(11)
We have previously shown that experimental infection caused by Trypanosoma cruzi
is associated with changes in the hypothalamus-pituitary-adrenal axis. Increased glucocorticoid (GC)
levels are believed to be protective against the effects of acute stress during infection but result
in depletion of CD4+CD8+ thymocytes by apoptosis, driving to thymic
atrophy. However, very few data are available concerning prolactin (PRL), another stress-related
hormone, which seems to be decreased during T. cruzi infection. Considering the
immunomodulatory role of PRL upon the effects caused by GC, we investigated if intrathymic
cross-talk between GC and PRL receptors (GR and PRLR, respectively) might influence T.
cruzi-induced thymic atrophy. Using an acute experimental model, we observed changes in
GR/PRLR cross-activation related with the survival of CD4+CD8+
thymocytes during infection. These alterations were closely related with systemic changes,
characterized by a stress hormone imbalance, with progressive GC augmentation simultaneously to PRL
reduction. The intrathymic hormone circuitry exhibited an inverse modulation that seemed to
counteract the GC-related systemic deleterious effects. During infection, adrenalectomy protected
the thymus from the increase in apoptosis ratio without changing PRL levels, whereas an additional
inhibition of circulating PRL accelerated the thymic atrophy and led to an increase in
corticosterone systemic levels. These results demonstrate that the PRL impairment during infection
is not caused by the increase of corticosterone levels, but the opposite seems to occur.
Accordingly, metoclopramide (MET)-induced enhancement of PRL secretion protected thymic atrophy in
acutely infected animals as well as the abnormal export of immature and potentially autoreactive
CD4+CD8+ thymocytes to the periphery. In conclusion, our findings
clearly show that Trypanosoma cruzi subverts mouse thymus homeostasis by altering
intrathymic and systemic stress-related endocrine circuitries with major consequences upon the
normal process of intrathymic T cell development. 相似文献
15.
Désio Aurélio Farias-de-Oliveira Vinícius Cotta-de-Almeida Déa Maria S. Villa-Verde Ingo Riederer Juliana de Meis Wilson Savino 《Memórias do Instituto Oswaldo Cruz》2013,108(7):825-831
Developing thymocytes interact with thymic epithelial cells (TECs) through cell-cell
interactions, TEC-derived secretory moieties and extracellular matrix (ECM)-mediated
interactions. These physiological interactions are crucial for normal thymocyte
differentiation, but can be disrupted in pathological situations. Indeed, there is severe
thymic atrophy in animals acutely infected with Trypanosoma cruzi due to
CD4+CD8+ thymocyte depletion secondary to caspase-mediated apoptosis, together with
changes in ECM deposition and thymocyte migration. We studied an in vitro model of TEC
infection by T. cruzi and found that infected TEC cultures show a reduced
number of cells, which was likely associated with decreased proliferative capacity, but
not with increased cell death, as demonstrated by bromodeoxyuridine and annexin-V
labelling. The infected TEC cultures exhibited increased expression of fibronectin (FN),
laminin (LM) and type IV collagen. Importantly, treatment with FN increased the relative
number of infected cells, whereas treatment with anti-FN or anti-LM antibodies resulted in
lower infection rates. Consistent with these data, we observed increased thymocyte
adhesion to infected TEC cultures. Overall, these results suggest that ECM molecules,
particularly FN, facilitate infection of the thymic epithelium and that the consequent
enhancement of ECM expression might be associated with changes in TEC-thymocyte
interactions. 相似文献
16.
Ana Luiza Cassin Duz Paula Melo de Abreu Vieira Bruno Mendes Roatt Rodrigo Dian Oliveira Aguiar-Soares Jamille Mirelle de Oliveira Cardoso Flávia Carvalho Bitencourt de Oliveira Levi Eduardo Soares Reis Washington Luiz Tafuri Vanja Maria Veloso Alexandre Barbosa Reis Cláudia Martins Carneiro 《Memórias do Instituto Oswaldo Cruz》2014,109(8):1005-1013
Trypanosoma cruzi infection may be caused by different strains with
distinct discrete typing units (DTUs) that can result in variable clinical forms of
chronic Chagas disease. The present study evaluates the immune response and cardiac
lesions in dogs experimentally infected with different T. cruzi
strains with distinct DTUs, namely, the Colombian (Col) and Y strains of TcI
and TcII DTU, respectively. During infection with the Col strain, increased levels of
alanine aminotransferase, erythrocytes, haematocrit and haemoglobin were observed. In
addition, CD8+ T-lymphocytes isolated from the peripheral blood produced
higher levels of interleukin (IL)-4. The latter suggests that during the acute phase,
infection with the Col strain may remain unnoticed by circulating mononuclear cells.
In the chronic phase, a significant increase in the number of inflammatory cells was
detected in the right atrium. Conversely, infection with the Y strain led to
leucopoenia, thrombopoenia, inversion of the ratio of CD4+/CD8+
T-lymphocytes and alterations in monocyte number. The Y strain stimulated the
production of interferon-γ by CD4+ and CD8+ T-lymphocytes and
IL-4 by CD8+ T-cells. In the chronic phase, significant heart inflammation
and fibrosis were observed, demonstrating that strains of different DTUs interact
differently with the host. 相似文献
17.
Maria T. Ronco Daniel E. Francés Paola I. Ingaramo Ariel D. Quiroga Maria L. Alvarez Gerardo B. Pisani Silvia S. Revelli Cristina E. Carnovale 《Cytokine》2010,49(1):64-72
Trypanosoma cruzi (T. cruzi) infected C57BL/6 mice developed a progressive fatal disease due to an imbalance in the profile of circulating related compounds accompanying infection like tumor necrosis factor alpha (TNFα). TNFα has been proposed as an important effector molecule in apoptosis. In this work, we evaluate inflammation and the proteins involved in apoptotic process in liver of infected mice and the role of TNFα. C57BL6/mice were infected subcutaneously with 100 viable trypomastigotes of Tulahuén strain of T cruzi. One set of these animals were treated with 375 μg of antihuman TNFα blocking antibody. Animals were sacrificed at 14 days post-infection (p.i).The analyses of Bcl-2 family proteins revealed an increase of the pro-apoptotic proteins Bax and tBid in T. cruzi-infected mice. Compared with control animals, cytochrome c release was increased. Apoptosis was also induced in infected mice. Anti-TNFα treatment decreases hepatic apoptosis. Our results suggest that T. cruzi infection induces programmed cell death in the host liver by increase of TNFα production, associated with TNF-R1 over-expression, that set in motion the Bid cleavage and mitochondrial translocation, Bax mitochondrial translocation, cytochrome c release, and ultimately apoptosis induction. 相似文献
18.
Torriceli Souza Thé Renata Siqueira Portella Marcos Lázaro Guerreiro Sonia Gumes Andrade 《Memórias do Instituto Oswaldo Cruz》2013,108(6):691-698
Acute infection with Trypanosoma cruzi results in intense
myocarditis, which progresses to a chronic, asymptomatic indeterminate form. The
evolution toward this chronic cardiac form occurs in approximately 30% of all
cases of T. cruzi infection. Suppression of delayed type
hypersensitivity (DTH) has been proposed as a potential explanation of the
indeterminate form. We investigated the effect of cyclophosphamide (CYCL)
treatment on the regulatory mechanism of DTH and the participation of heart
interstitial dendritic cells (IDCs) in this process using BALB/c mice
chronically infected with T. cruzi. One group was treated with
CYCL (20 mg/kg body weight) for one month. A DTH skin test was performed by
intradermal injection of T. cruzi antigen (3 mg/mL) in the
hind-footpad and measured the skin thickness after 24 h, 48 h and 72 h. The skin
test revealed increased thickness in antigen-injected footpads, which was more
evident in the mice treated with CYCL than in those mice that did not receive
treatment. The thickened regions were characterised by perivascular infiltrates
and areas of necrosis. Intense lesions of the myocardium were present in
three/16 cases and included large areas of necrosis. Morphometric evaluation of
lymphocytes showed a predominance of TCD8 cells. Heart IDCs were immunolabelled
with specific antibodies (CD11b and CD11c) and T. cruzi
antigens were detected using a specific anti-T. cruzi antibody.
Identification of T. cruzi antigens, sequestered in these cells
using specific anti-T. cruzi antibodies was done, showing a
significant increase in the number of these cells in treated mice. These results
indicate that IDCs participate in the regulatory mechanisms of DTH response to
T. cruzi infection. 相似文献
19.
Claudia Mendon?a Bezerra Luciano Pamplona de Góes Cavalcanti Rita de Cássia Moreira de Souza Silvia Ermelinda Barbosa Samanta Cristina das Chagas Xavier Ana Maria Jansen Relrison Dias Ramalho Liléia Diotaiut 《Memórias do Instituto Oswaldo Cruz》2014,109(7):887-898
The role played by different mammal species in the maintenance of Trypanosoma
cruzi is not constant and varies in time and place. This study aimed to
characterise the importance of domestic, wild and peridomestic hosts in the
transmission of T. cruzi in Tauá, state of Ceará, Caatinga area,
Brazil, with an emphasis on those environments colonised by Triatoma
brasiliensis. Direct parasitological examinations were performed on
insects and mammals, serologic tests were performed on household and outdoor mammals
and multiplex polymerase chain reaction was used on wild mammals. Cytochrome b was
used as a food source for wild insects. The serum prevalence in dogs was 38% (20/53),
while in pigs it was 6% (2/34). The percentages of the most abundantly infected wild
animals were as follows: Thrichomys laurentius 74% (83/112)
and Kerodon rupestris 10% (11/112). Of the 749 triatomines
collected in the household research, 49.3% (369/749) were positive for T.
brasiliensis, while 6.8% were infected with T. cruzi
(25/369). In captured animals, T. brasiliensis shares a
natural environment with T. laurentius, K.
rupestris, Didelphis albiventris, Monodelphis
domestica, Galea spixii, Wiedomys
pyrrhorhinos, Conepatus semistriatus and Mus
musculus. In animals identified via their food
source, T. brasiliensis shares a natural environment with
G. spixii, K. rupestris, Capra hircus, Gallus
gallus, Tropidurus oreadicus and Tupinambis merianae.
The high prevalence of T. cruzi in household and peridomiciliar
animals reinforces the narrow relationship between the enzootic cycle and humans in
environments with T. brasiliensis and characterises it as
ubiquitous. 相似文献
20.
Trypanosoma cruzi triggers a progressive myocarditis in mammalians through activation and recruitment of leukocytes and release of inflammatory mediators. The chemokine CX3CL1 has been highlighted for its potential role in the parasite controlling in end-pathological status of infected hosts. This study investigated the systemic and cardiac release of CX3CL1 in experimental T. cruzi infection and how this chemokine correlates with endothelin-1 and TNF. Male Fisher rats (n = 20) were infected, or not, by the Y strain of T. cruzi and parasitemia was daily evaluated and immunoassays performed in the cardiac tissue macerated supernatant and in serum to evaluate CX3CL1, endothelin, and TNF production on days 5 and 15 of infection. T. cruzi infection induced a higher serum and cardiac production of these mediators on days 5 and 15 of infection. In both periods of infection, respectively, CX3CL1 showed a positive correlation with TNF (r = 0.833, p < 0.001 and r = 0.723, p < 0.001) and endothelin-1 (r = 0.801, p < 0.05 and r = 0.857, p < 0.001), which reinforce its participation in the T. cruzi-induced myocarditis development. 相似文献