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Cerebral malaria

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https://www.readbyqxmd.com/read/28500775/vaccines-against-malaria-still-a-long-way-to-go
#1
REVIEW
Kai Matuschewski
Several species of Plasmodium cause a broad spectrum of human disease that range from nausea and fever to severe anemia, cerebral malaria, and multi-organ failure. In malaria-endemic countries continuous exposure to Plasmodium sporozoite inoculations and subsequent blood infections elicit only partial and short-lived immunity, which gradually develops over many years of parasite exposure and multiple clinical episodes. The ambitious goal of malaria vaccinology over the past 70 years has been to develop an immunization strategy that mounts protection superior to naturally acquired immunity...
May 13, 2017: FEBS Journal
https://www.readbyqxmd.com/read/28475625/plasmodium-falciparum-histidine-rich-protein-ii-causes-vascular-leakage-and-exacerbates-experimental-cerebral-malaria-in-mice
#2
Priya Pal, Amanda E Balaban, Michael S Diamond, Photini Sinnis, Robyn S Klein, Daniel E Goldberg
A devastating complication of Plasmodium falciparum infection is cerebral malaria, in which vascular leakage and cerebral swelling lead to coma and often death. P. falciparum produces a protein called histidine-rich protein II (HRPII) that accumulates to high levels in the bloodstream of patients and serves as a diagnostic and prognostic marker for falciparum malaria. Using a human cerebral microvascular endothelial barrier model, we previously found that HRPII activates the endothelial cell inflammasome, resulting in decreased integrity of tight junctions and increased endothelial barrier permeability...
2017: PloS One
https://www.readbyqxmd.com/read/28454880/expression-of-negative-immune-regulatory-molecules-pro-inflammatory-chemokine-and-cytokines-in-immunopathology-of-ecm-developing-mice
#3
Ashwin V Khandare, Deepali Bobade, Mangesh Deval, Tushar Patil, Bhaskar Saha, D Prakash
The pathological events in human cerebral malaria are mimicked in the experimental cerebral malaria (ECM) in Plasmodium berghei ANKA (PBA)-infected C57BL/6 mice. Although previously implied in ECM, the kinetics of cytokines and chemokines expression-an essential functional feature for defining causality in ECM development-remained untested. Herein, we characterized the immunopathological changes and the expression of negative immune regulatory molecules, cytokines and chemokines through asymptomatic (3days after infection, 3dpi), symptomatic (5dpi) and ECM (7dpi) stages in PBA-infected C57BL/6 mice...
April 25, 2017: Acta Tropica
https://www.readbyqxmd.com/read/28453871/elevated-cerebrospinal-fluid-tumor-necrosis-factor-is-associated-with-acute-and-long-term-neurocognitive-impairment-in-cerebral-malaria
#4
Estela Shabani, Benson J Ouma, Richard Idro, Paul Bangirana, Robert O Opoka, Gregory S Park, Andrea L Conroy, Chandy C John
Systemic tumor necrosis factor-α (TNF-α) may contribute to the pathogenesis of cerebral malaria (CM) by promoting endothelial activation and parasite sequestration. However less is known about the role of central nervous system (CNS) TNF-α in CM. We assessed plasma (n=249) and cerebrospinal fluid (CSF) (n=167) TNF-α levels in Ugandan children with CM, plasma TNF-α in Ugandan community control children (n=198), and CSF TNF-α in North American control children who had recovered from leukemia (n=13). Plasma and CSF TNF-α were measured by magnetic bead assay...
April 28, 2017: Parasite Immunology
https://www.readbyqxmd.com/read/28452684/dynamic-interactions-of-plasmodium-spp-with-vascular-endothelium
#5
Mark R Gillrie, May Ho
Plasmodial species are protozoan parasites that infect erythrocytes. As such, they are in close contact with microvascular endothelium for most of the life cycle in the mammalian host. The host-parasite interactions of this stage of the infection are responsible for the clinical manifestations of the disease that range from a mild febrile illness to severe and frequently fatal syndromes such as cerebral malaria and multi-organ failure. Plasmodium falciparum, the causative agent of the most severe form of malaria, is particularly predisposed to modulating endothelial function through either direct adhesion to endothelial receptor molecules, or by releasing potent host and parasite products that can stimulate endothelial activation and/or disrupt barrier function...
January 2, 2017: Tissue Barriers
https://www.readbyqxmd.com/read/28448579/il-33-receptor-st2-regulates-the-cognitive-impairments-associated-with-experimental-cerebral-malaria
#6
Flora Reverchon, Stéphane Mortaud, Maëliss Sivoyon, Isabelle Maillet, Anthony Laugeray, Jennifer Palomo, Céline Montécot, Améziane Herzine, Sandra Meme, William Meme, François Erard, Bernhard Ryffel, Arnaud Menuet, Valérie F J Quesniaux
Cerebral malaria (CM) is associated with a high mortality rate and long-term neurocognitive impairment in survivors. The murine model of experimental cerebral malaria (ECM) induced by Plasmodium berghei ANKA (PbA)-infection reproduces several of these features. We reported recently increased levels of IL-33 protein in brain undergoing ECM and the involvement of IL-33/ST2 pathway in ECM development. Here we show that PbA-infection induced early short term and spatial memory defects, prior to blood brain barrier (BBB) disruption, in wild-type mice, while ST2-deficient mice did not develop cognitive defects...
April 2017: PLoS Pathogens
https://www.readbyqxmd.com/read/28426698/extensive-alterations-of-blood-metabolites-in-pediatric-cerebral-malaria
#7
Sanchit Gupta, Karl Seydel, Miguel A Miranda-Roman, Catherine M Feintuch, Alex Saidi, Ryung S Kim, Gretchen L Birbeck, Terrie Taylor, Johanna P Daily
Cerebral malaria (CM) presents as an encephalopathy and is due to infection with Plasmodium falciparum. Patients are comatose, often with fever, recurrent seizures and this condition is associated with a high mortality rate. The etiology of the coma and seizures are poorly understood. Circulating small molecules and lipids have bioactive functions and alterations in their concentrations have been implicated in seizure disorders and other forms of encephalopathy. We carried out a comprehensive analysis of blood metabolites during CM to explore a biochemical basis of this encephalopathy...
2017: PloS One
https://www.readbyqxmd.com/read/28416929/role-of-coma-acidosis-malaria-score-in-patients-with-severe-malaria-among-indian-population-a-tertiary-care-center-experience
#8
Hari Krishan Aggarwal, Deepak Jain, Avinash Rao, Rajinish Kalra
OBJECTIVE: Malaria is a prime public health threat in developing countries like India. There is an unmet need of a simplified methodology for the purpose of triage and provision of intensive care to the severely infected patients in these areas. MATERIALS AND METHODS: We did a prospective study in patients (n=60) admitted with severe malaria in a single tertiary care center in the state of Haryana, India. We assessed the role of coma acidosis malaria (CAM) score in these patients when predicting mortality and morbidity events...
February 2017: Eurasian Journal of Medicine
https://www.readbyqxmd.com/read/28414649/gaining-ground-against-cerebral-malaria
#9
Adrian Burton
No abstract text is available yet for this article.
May 2017: Lancet Neurology
https://www.readbyqxmd.com/read/28413714/cerebrospinal-fluid-and-plasma-%C3%AE-endorphin-levels-in-children-with-cerebral-malaria
#10
Oluwatosin Eunice Olorunmoteni, Oluwagbemiga Oyewole Adeodu, Saheed B A Oseni, Efere M Obuotor
OBJECTIVES: Cerebral malaria (CM) is the most lethal form of malaria, yet its pathogenesis is not fully understood. Cytoadherence, sequestration, alterations in cytokine expression, inflammation, and microvascular obstruction are all hypothesized to be important in the aetio-pathogenesis of coma which characterizes cerebral malaria and the death which sometimes result. Beta (β)-endorphin has been postulated to be involved in the pathogenetic processes of inflammation and cytokine expression, although the exact role is unknown...
April 2017: Brain and Behavior
https://www.readbyqxmd.com/read/28396319/host-resistance-to-plasmodium-induced-acute-immune-pathology-is-regulated-by-il-10-receptor-signalling
#11
Carla Claser, J Brian De Souza, Samuel G Thorburn, Georges Emile Grau, Eleanor M Riley, Laurent Rénia, Julius C R Hafalla
The resolution of malaria infection is dependent on a balance between pro-inflammatory and regulatory immune responses. Whilst early effector T cell responses are required for limiting parasitaemia, these responses need to be switched off by regulatory mechanisms in a timely manner to avoid immune-mediated tissue damage. Interleukin-10 (IL-10) receptor (IL-10R) signalling is considered to be a vital component of regulatory responses although its role in host resistance to severe immune pathology during acute malaria infections is not fully understood...
April 10, 2017: Infection and Immunity
https://www.readbyqxmd.com/read/28339598/high-postdischarge-morbidity-in-ugandan-children-with-severe-malarial-anemia-or-cerebral-malaria
#12
Robert O Opoka, Karen E S Hamre, Nathan Brand, Paul Bangirana, Richard Idro, Chandy C John
Summary: Postdischarge readmission and outpatient illnesses are frequent in children with severe malarial anemia or cerebral malaria. Trials of postdischarge malaria prophylaxis in children with severe malaria should be considered. Background: Cerebral malaria (CM) and severe malarial anemia (SMA) account for a substantial proportion of malaria-related deaths in sub-Saharan Africa. However, postdischarge morbidity in children with CM or SMA has not been well established...
October 7, 2016: Journal of the Pediatric Infectious Diseases Society
https://www.readbyqxmd.com/read/28336326/oxidative-stress-and-genes-regulation-of-cerebral-malaria-upon-zizyphus-spina-christi-treatment-in-a-murine-model
#13
Murad A Mubaraki, Taghreed A Hafiz, Saleh Al-Quraishy, Mohamed A Dkhil
The development and spread of multidrug-resistant strains of malarial parasites have led to an overwhelming increase in the resistance to current antimalarial drugs. The urgent need for alternative antimalarial drugs has directed some of the current studies toward folkloric medicine approaches. Interestingly, the Zizyphus spina Cristi leaf extract (ZLE) has been found to exhibit antiplasmodial activity. This study evaluated the protective effect of ZLE against Plasmodium berghei-induced cerebral tissue injuries in mice...
March 21, 2017: Microbial Pathogenesis
https://www.readbyqxmd.com/read/28318894/synthesis-and-human-bacterial-carbonic-anhydrase-inhibition-with-a-series-of-sulfonamides-incorporating-phthalimido-moieties
#14
Menshawy A Mohamed, Alaa A-M Abdel-Aziz, Helmy M Sakr, Adel S El-Azab, Silvia Bua, Claudiu T Supuran
A series of sulfonamides was obtained by reacting substituted-2-(1,3-dioxo-1,3-dihydroisobenzofuran-5-carboxamido)benzoic acids with aromatic sulfonamides incorporating primary amino moieties. The new compounds were investigated as inhibitor of four carbonic anhydrase (CA, EC 4.2.1.1) isoforms, the human (h) hCA I and II, and the α- and β-class CAs from the pathogenic bacterium Vibrio cholerae, VchCAα and VhcCAβ. hCA I was effectively inhibited by the new sulfonamides, with inhibition constants in the range of 4...
March 9, 2017: Bioorganic & Medicinal Chemistry
https://www.readbyqxmd.com/read/28279348/structure-guided-identification-of-a-family-of-dual-receptor-binding-pfemp1-that-is-associated-with-cerebral-malaria
#15
Frank Lennartz, Yvonne Adams, Anja Bengtsson, Rebecca W Olsen, Louise Turner, Nicaise T Ndam, Gertrude Ecklu-Mensah, Azizath Moussiliou, Michael F Ofori, Benoit Gamain, John P Lusingu, Jens E V Petersen, Christian W Wang, Sofia Nunes-Silva, Jakob S Jespersen, Clinton K Y Lau, Thor G Theander, Thomas Lavstsen, Lars Hviid, Matthew K Higgins, Anja T R Jensen
Cerebral malaria is a deadly outcome of infection by Plasmodium falciparum, occurring when parasite-infected erythrocytes accumulate in the brain. These erythrocytes display parasite proteins of the PfEMP1 family that bind various endothelial receptors. Despite the importance of cerebral malaria, a binding phenotype linked to its symptoms has not been identified. Here, we used structural biology to determine how a group of PfEMP1 proteins interacts with intercellular adhesion molecule 1 (ICAM-1), allowing us to predict binders from a specific sequence motif alone...
March 8, 2017: Cell Host & Microbe
https://www.readbyqxmd.com/read/28273147/a-quantitative-brain-map-of-experimental-cerebral-malaria-pathology
#16
Patrick Strangward, Michael J Haley, Tovah N Shaw, Jean-Marc Schwartz, Rachel Greig, Aleksandr Mironov, J Brian de Souza, Sheena M Cruickshank, Alister G Craig, Danny A Milner, Stuart M Allan, Kevin N Couper
The murine model of experimental cerebral malaria (ECM) has been utilised extensively in recent years to study the pathogenesis of human cerebral malaria (HCM). However, it has been proposed that the aetiologies of ECM and HCM are distinct, and, consequently, no useful mechanistic insights into the pathogenesis of HCM can be obtained from studying the ECM model. Therefore, in order to determine the similarities and differences in the pathology of ECM and HCM, we have performed the first spatial and quantitative histopathological assessment of the ECM syndrome...
March 2017: PLoS Pathogens
https://www.readbyqxmd.com/read/28272506/a-murine-model-to-study-epilepsy-and-sudep-induced-by-malaria-infection
#17
Paddy Ssentongo, Anna E Robuccio, Godfrey Thuku, Derek G Sim, Ali Nabi, Fatemeh Bahari, Balaji Shanmugasundaram, Myles W Billard, Andrew Geronimo, Kurt W Short, Patrick J Drew, Jennifer Baccon, Steven L Weinstein, Frank G Gilliam, José A Stoute, Vernon M Chinchilli, Andrew F Read, Bruce J Gluckman, Steven J Schiff
One of the largest single sources of epilepsy in the world is produced as a neurological sequela in survivors of cerebral malaria. Nevertheless, the pathophysiological mechanisms of such epileptogenesis remain unknown and no adjunctive therapy during cerebral malaria has been shown to reduce the rate of subsequent epilepsy. There is no existing animal model of postmalarial epilepsy. In this technical report we demonstrate the first such animal models. These models were created from multiple mouse and parasite strain combinations, so that the epilepsy observed retained universality with respect to genetic background...
March 8, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28264905/perforin-expression-by-cd8-t-cells-is-sufficient-to-cause-fatal-brain-edema-during-experimental-cerebral-malaria
#18
Matthew A Huggins, Holly L Johnson, Fang Jin, Aurelie N Songo, Lisa M Hanson, Stephanie J LaFrance, Noah S Butler, John T Harty, Aaron J Johnson
Human cerebral malaria (HCM) is a serious complication of Plasmodium falciparum infection. The most severe outcomes for patients include coma, permanent neurological deficits, and death. Recently, a large-scale magnetic resonance imaging (MRI) study in humans identified brain swelling as the most prominent predictor of fatal HCM. Therefore, in this study, we sought to define the mechanism controlling brain edema through the use of the murine experimental cerebral malaria (ECM) model. Specifically, we investigated the ability of CD8 T cells to initiate brain edema during ECM...
May 2017: Infection and Immunity
https://www.readbyqxmd.com/read/28261571/targeting-angiotensin-ii-type-1-receptor-at1r-inhibits-the-harmful-phenotype-of-plasmodium-specific-cd8-t-cells-during-blood-stage-malaria
#19
João L Silva-Filho, Celso Caruso-Neves, Ana A S Pinheiro
CD8(+) T-cell response is critical in the pathogenesis of cerebral malaria during blood-stage. Our group and other have been shown that angiotensin II (Ang II) and its receptor AT1 (AT1R), a key effector axis of renin-angiotensin system (RAS), have immune regulatory effects on T cells. Previously, we showed that inhibition of AT1R signaling protects mice against the lethal disease induced by Plasmodium berghei ANKA infection However, most of the Ang II/AT1R actions were characterized by using only pharmacological approaches, the effects of which may not always be due to a specific receptor blockade...
2017: Frontiers in Cellular and Infection Microbiology
https://www.readbyqxmd.com/read/28249591/controlled-release-of-artemisone-for-the-treatment-of-experimental-cerebral-malaria
#20
Jacob Golenser, Viola Buchholz, Amir Bagheri, Abed Nasereddin, Ron Dzikowski, Jintao Guo, Nicholas H Hunt, Sara Eyal, Natalia Vakruk, Andreas Greiner
BACKGROUND: Cerebral malaria (CM) is a leading cause of malarial mortality resulting from infection by Plasmodium falciparum. Treatment commonly involves adjunctive care and injections or transfusion of artemisinins. All artemisinins that are in current use are metabolized to dihydroxyartemisinin (DHA), to which there is already some parasite resistance. We used artemisone, a derivative that does not convert to DHA, has improved pharmacokinetics and anti-plasmodial activity and is also anti-inflammatory (an advantage given the immunopathological nature of CM)...
March 1, 2017: Parasites & Vectors
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