Cytoadherence of Plasmodium berghei-Infected Red Blood Cells to Murine Brain and Lung Microvascular Endothelial Cells<i>In Vitro</i>

El‐Assaad, Fatima; Wheway, Julie; Mitchell, Andrew J.; Lou, Jinning; Hunt, Nicholas H.; Combes, Valéry; Grau, Georges E.

doi:10.1128/iai.00428-13

Cited by 51 publications

(44 citation statements)

References 86 publications

(118 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…IL-10 suppresses a Th1 response and has been shown in multiple studies to play a major role in preventing ECM (28,33,34,75). To investigate whether STAg-induced protection against ECM requires IL-10, we infected IL-10 Ϫ/Ϫ mice with P. berghei ANKA and treated mice with STAg after 24 h. STAg treatment was just as effective in wild-type (wt) and IL-10 Ϫ/Ϫ mice, as evidenced by similar percent survivals (Fig.…”

Section: Stag Treatment Alone and Stag Treatment Of P Berghei-infecmentioning

confidence: 99%

Toxoplasma gondii Upregulates Interleukin-12 To Prevent Plasmodium berghei-Induced Experimental Cerebral Malaria

et al. 2014

View full text Add to dashboard Cite

A chronic infection with the parasite Toxoplasma gondii has previously been shown to protect mice against subsequent viral, bacterial, or protozoal infections. Here we have shown that a chronic T. gondii infection can prevent Plasmodium berghei ANKA-induced experimental cerebral malaria (ECM) in C57BL/6 mice. Treatment with soluble T. gondii antigens (STAg) reduced parasite sequestration and T cell infiltration in the brains of P. berghei-infected mice. Administration of STAg also preserved blood-brain barrier function, reduced ECM symptoms, and significantly decreased mortality. STAg treatment 24 h post-P. berghei infection led to a rapid increase in serum levels of interleukin 12 (IL-12) and gamma interferon (IFN-␥). By 5 days after P. berghei infection, STAg-treated mice had reduced IFN-␥ levels compared to those of mock-treated mice, suggesting that reductions in IFN-␥ at the time of ECM onset protected against lethality. Using IL-10-and IL-12␤R-deficient mice, we found that STAg-induced protection from ECM is IL-10 independent but IL-12 dependent. Treatment of P. berghei-infected mice with recombinant IL-12 significantly decreased parasitemia and mortality. These data suggest that IL-12, either induced by STAg or injected as a recombinant protein, mediates protection from ECM-associated pathology potentially through early induction of IFN-␥ and reduction in parasitemia. These results highlight the importance of early IL-12 induction in protection against ECM.

show abstract

Section: Stag Treatment Alone and Stag Treatment Of P Berghei-infecmentioning

confidence: 99%

Toxoplasma gondii Upregulates Interleukin-12 To Prevent Plasmodium berghei-Induced Experimental Cerebral Malaria

et al. 2014

View full text Add to dashboard Cite

show abstract

“…In accordance with the bacterial colonization capacity in vivo, we used the human laryngeal carcinoma cell line HEp-2 and mouse brain microvascular endothelial cells (bEnd.3) as in the models of bacterial colonization (19,20,23) and meningitis (24,25) in vitro, respectively. The adherence assays were performed as previously described (26).…”

mentioning

confidence: 99%

Novel Variant Serotype of Streptococcus suis Isolated from Piglets with Meningitis

Pan

Wang³

et al. 2015

Appl Environ Microbiol

View full text Add to dashboard Cite

cStreptococcus suis is an emerging zoonotic pathogen causing severe infections in pigs and humans. In previous studies, 33 serotypes of S. suis have been identified using serum agglutination. Here, we describe a novel S. suis strain, CZ130302, isolated from an outbreak of acute piglet meningitis in eastern China. Strong pathogenicity of meningitis caused by strain CZ130302 was reproduced in the BALB/c mouse model. The strain showed a high fatality rate (8/10), higher than those for known virulent serotype 2 strains P1/7 (1/10) and 9801 (2/10). Cell adhesion assay results with bEnd.3 and HEp2 cells showed that CZ130302 was significantly close to P1/7 and 9801. Both the agglutination test and its complementary test showed that strain CZ130302 had no strong cross-reaction with the other 33 S. suis serotypes. The multiplex PCR assays revealed no specified bands for all four sets used to detect the other 33 serotypes. In addition, genetic analysis of the whole cps gene clusters of all serotypes was performed in this study. The results of comparative genomics showed that the cps gene cluster of CZ130302, which was not previously reported, showed no homology to the gene sequences of the other strains. Especially, the wzy, wzx, and acetyltransferase genes of strain CZ130302 are phylogenetically distinct from strains of the other 33 serotypes. Therefore, this study suggested that strain CZ130302 represents a novel variant serotype of S. suis (designated serotype Chz) which has a high potential to be virulent and associated with meningitis in animals. Streptococcus suis causes meningitis and septicemia in pigs and is also known as a zoonotic agent (1). Human infections of S. suis were first reported in Denmark in 1968 (2). Since then, this pathogen has spread all over the world. The human Streptococcus suis was epidemic in most Europe countries (3, 4), as well as in Asian countries, such as Vietnam and Thailand (5-7). In China, two outbreaks of human streptococcosis have occurred, affecting more than 100 people and causing 39 deaths (8). More and more S. suis infections from China, Thailand, Hong Kong, Taiwan, and Singapore have been reported, which indicates that S. suis has been an important cause of adult meningitis, endocarditis, septicemia, and arthritis in Asia (9).The serotyping of S. suis isolates rests on the basis of the antigenicity of their capsular polysaccharides (CPs); 35 serotypes have been identified by agglutination tests (10). With the development of sequence analysis of 16S rRNA and cpn60 genes in S. suis, the original S. suis serotypes 32 and 34 were reclassified as Streptococcus orisratti (11). Phylogenetic analyses of the cps gene cluster, conserved Wzy polymerase, Wzx flippase, and glycosyltransferase are all taken as important means of classifying a novel serotype (12). Multiplex PCR assays against the specific genes of the cps clusters have also been developed to identify serotypes in S. suis (13)(14)(15).From March to May 2013, strain CZ130302 caused an outbreak of streptococcosis in piglets at ...

show abstract

“…Plasmodium species incapable of forming knobs in infected erythrocytes (knobless Plasmodium) show a passive adhesion of infected RBCs to activated endothelial cells [75]. Thus, knobless Plasmodium activates endothelial cells to the same extent as knob-forming Plasmodium [66,73], which suggests that ECM may also be induced by parasitized erythrocytes.…”

Section: Inflammatory Components In the Development Of Cerebral Malariamentioning

confidence: 99%

“…Several findings observed in human cerebral malaria are also observed in experimental models, including cytokine activity [70], endothelial activation [71], and edema formation [72]; however, the sequestration of parasitized erythrocytes during experimental cerebral malaria (ECM) is not well understood. Recent evidence showed that Plasmodium berghei-ANKA infected RBCs adhere to brain microvascular endothelial cells in a VCAM-1-dependent manner [73]. In addition, another study suggests transient contact between infected RBCs and the endothelium [74].…”

Section: Inflammatory Components In the Development Of Cerebral Malariamentioning

confidence: 99%

Multiple Organ Dysfunction During Severe Malaria: The Role of the Inflammatory Response

Souza¹,

Pádua²,

Henriques³

2016

Current Topics in Malaria

View full text Add to dashboard Cite

Severe malaria is a systemic illness characterized by the dysfunction of one or more peripheral organs, such as the lungs [acute respiratory distress syndrome (ARDS)] and kidneys [acute kidney injury (AKI)]. Several clinical and experimental studies suggest that features of the inflammatory response are related to the multi-organ dysfunction observed in severe malaria. Our group has been dedicated to studying the roles of proand anti-inflammatory mediators in the multi-organ dysfunction observed in experimental severe malaria, especially in the lungs, kidneys, and brain. Herein, we explore severe malaria as a pathology derived from intense inflammatory responses in different organs and further distinguish and compare these organ-specific inflammatory responses. The pathophysiological mechanism of severe malaria is not fully elucidated; however, it is important to study it as a complex inflammatory response assembled by different actors, each one orchestrating a different mechanism.

show abstract

Cytoadherence of Plasmodium berghei-Infected Red Blood Cells to Murine Brain and Lung Microvascular Endothelial CellsIn Vitro

Cited by 51 publications

References 86 publications

Toxoplasma gondii Upregulates Interleukin-12 To Prevent Plasmodium berghei-Induced Experimental Cerebral Malaria

Toxoplasma gondii Upregulates Interleukin-12 To Prevent Plasmodium berghei-Induced Experimental Cerebral Malaria

Novel Variant Serotype of Streptococcus suis Isolated from Piglets with Meningitis

Multiple Organ Dysfunction During Severe Malaria: The Role of the Inflammatory Response

Contact Info

Product

Resources

About