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Journal articles on the topic 'Malaria – Pathogenesis'

Author: Grafiati

Published: 4 June 2021

Last updated: 6 September 2023

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1

Milner, Danny A. "Malaria Pathogenesis." Cold Spring Harbor Perspectives in Medicine 8, no. 1 (May 22, 2017): a025569. http://dx.doi.org/10.1101/cshperspect.a025569.

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2

Miller, L., M. Good, and G. Milon. "Malaria pathogenesis." Science 264, no. 5167 (June 24, 1994): 1878–83. http://dx.doi.org/10.1126/science.8009217.

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3

Amoako-Sakyi, Daniel, Selorme Adukpo, Kwadwo A. Kusi, Daniel Dodoo, Michael F. Ofori, George O. Adjei, Dominic E. Edoh, et al. "A STAT6 Intronic Single-Nucleotide Polymorphism is Associated with Clinical Malaria in Ghanaian Children." Genetics & Epigenetics 8 (January 2016): GEG.S38307. http://dx.doi.org/10.4137/geg.s38307.

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Malaria pathogenesis may be influenced by IgE responses and cytokine cross-regulation. Several mutations in the IL-4/STAT6 signaling pathway can alter cytokine cross-regulation and IgE responses during a Plasmodium falciparum malarial infection. This study investigated the relationship between a STAT6 intronic single-nucleotide polymorphism (rs3024974), total IgE, cytokines, and malaria severity in 238 Ghanaian children aged between 0.5 and 13 years. Total IgE and cytokine levels were measured by ELISA, while genotyping was done by polymerase chain reaction-restriction fragment length polymorp

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4

John, Chandy C. "Cerebral Malaria Pathogenesis." American Journal of Pathology 171, no. 6 (December 2007): 1729–32. http://dx.doi.org/10.2353/ajpath.2007.070917.

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5

Clark, I. A., and L. Schofield. "Pathogenesis of Malaria." Parasitology Today 16, no. 10 (October 2000): 451–54. http://dx.doi.org/10.1016/s0169-4758(00)01757-9.

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6

Mideo, Nicole, Troy Day, and Andrew F. Read. "Modelling malaria pathogenesis." Cellular Microbiology 10, no. 10 (October 2008): 1947–55. http://dx.doi.org/10.1111/j.1462-5822.2008.01208.x.

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O’Sullivan, Jamie M., and James S. O’Donnell. "Platelets in malaria pathogenesis." Blood 132, no. 12 (September 20, 2018): 1222–24. http://dx.doi.org/10.1182/blood-2018-08-865618.

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8

Dasari, Prasad, and Sucharit Bhakdi. "Pathogenesis of malaria revisited." Medical Microbiology and Immunology 201, no. 4 (September 7, 2012): 599–604. http://dx.doi.org/10.1007/s00430-012-0265-y.

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9

Meshnick, Steven R., and Stephen J. Rogerson. "Pathogenesis of malaria in pregnancy." Microbiology Australia 29, no. 4 (2008): 204. http://dx.doi.org/10.1071/ma08204.

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Even though we have good tools to prevent and treat malaria, it remains a tragically common disease in poor countries, especially in Africa. Pregnant women are particularly susceptible to malaria, causing anaemia and poor birth outcomes. There is marked sequestration of Plasmodium falciparum-infected erythrocytes (IEs) in the placenta, but the pathogenesis of malaria in pregnancy is still incompletely understood. Both intermittent preventive therapy and insecticide-impregnated bed nets are effective protective measures, but new measures are also needed.

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Moxon, Christopher A., Matthew P. Gibbins, Dagmara McGuinness, Danny A. Milner, and Matthias Marti. "New Insights into Malaria Pathogenesis." Annual Review of Pathology: Mechanisms of Disease 15, no. 1 (January 24, 2020): 315–43. http://dx.doi.org/10.1146/annurev-pathmechdis-012419-032640.

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Malaria remains a major public health threat in tropical and subtropical regions across the world. Even though less than 1% of malaria infections are fatal, this leads to about 430,000 deaths per year, predominantly in young children in sub-Saharan Africa. Therefore, it is imperative to understand why a subset of infected individuals develop severe syndromes and some of them die and what differentiates these cases from the majority that recovers. Here, we discuss progress made during the past decade in our understanding of malaria pathogenesis, focusing on the major human parasite Plasmodium f

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Mandala, Wilson L., Chisomo L. Msefula, Esther N. Gondwe, James J. Gilchrist, Stephen M. Graham, Paul Pensulo, Grace Mwimaniwa, et al. "Lymphocyte Perturbations in Malawian Children with Severe and Uncomplicated Malaria." Clinical and Vaccine Immunology 23, no. 2 (November 18, 2015): 95–103. http://dx.doi.org/10.1128/cvi.00564-15.

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ABSTRACTLymphocytes are implicated in immunity and pathogenesis of severe malaria. Since lymphocyte subsets vary with age, assessment of their contribution to different etiologies can be difficult. We immunophenotyped peripheral blood from Malawian children presenting with cerebral malaria, severe malarial anemia, and uncomplicated malaria (n= 113) and healthy aparasitemic children (n= 42) in Blantyre, Malawi, and investigated lymphocyte subset counts, activation, and memory status. Children with cerebral malaria were older than those with severe malarial anemia. We found panlymphopenia in chi

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12

Chang, Wun-Ling, Jie Li, Guang Sun, Hong-Li Chen, Robert D. Specian, Seth Mark Berney, D. Neil Granger, and Henri C. van der Heyde. "P-Selectin Contributes to Severe Experimental Malaria but Is Not Required for Leukocyte Adhesion to Brain Microvasculature." Infection and Immunity 71, no. 4 (April 2003): 1911–18. http://dx.doi.org/10.1128/iai.71.4.1911-1918.2003.

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ABSTRACT Plasmodium berghei-infected mice, a well-recognized model of experimental cerebral malaria (ECM), exhibit many of the hallmarks of a systemic inflammatory response, with organ damage in brain, lung, and kidneys. Identification of the molecules mediating pathogenesis of the inflammatory response, such as leukocyte adhesion, may lead to new therapies. Indeed, mice lacking the cell adhesion molecule P-selectin were significantly (P = 0.005) protected from death due to P. berghei malaria compared with C57BL/6 controls despite similar parasitemia (P = 0.6) being found in both groups of mic

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13

English, Mike, and Kevin Marsh. "Childhood malaria – pathogenesis and treatment." Current Opinion in Infectious Diseases 10, no. 3 (June 1997): 221–25. http://dx.doi.org/10.1097/00001432-199706000-00011.

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14

Fujioka, H., and M. Aikawa. "Molecular Pathogenesis of Cerebral Malaria." Microscopy and Microanalysis 3, S2 (August 1997): 39–40. http://dx.doi.org/10.1017/s143192760000708x.

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Plasmodium falciparum, the most malignant human malaria, is responsible for 2-3 million deaths annually. These infections often involve blockage of the cerebral microvasculature by P. falciparum-infected erythrocytes (Fig. 1). This aspect is considered the major factor in the pathogenesis of cerebral malaria.Upon invasion of the erythrocyte, P. falciparum immediately begins to remodel the infected erythrocyte. The adherence points of infected erythrocytes, termed knobs (Fig. 2 and 3), contain antigenically diverse 200-350kDa surface proteins (PfEMPl; Fig. 4). The PfEMPl variant surface protein

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Antia, Meher, Thurston Herricks, and Pradipsinh K. Rathod. "Microfluidic approaches to malaria pathogenesis." Cellular Microbiology 10, no. 10 (October 2008): 1968–74. http://dx.doi.org/10.1111/j.1462-5822.2008.01216.x.

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16

Schofield, Louis, and Georges E. Grau. "Immunological processes in malaria pathogenesis." Nature Reviews Immunology 5, no. 9 (September 2005): 722–35. http://dx.doi.org/10.1038/nri1686.

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Rasti, Niloofar, Mats Wahlgren, and Qijun Chen. "Molecular aspects of malaria pathogenesis." FEMS Immunology & Medical Microbiology 41, no. 1 (May 2004): 9–26. http://dx.doi.org/10.1016/j.femsim.2004.01.010.

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18

Verhoef, Hans, Clive E. West, Rob Kraaijenhagen, Silas M. Nzyuko, Rose King, Mary M. Mbandi, Susanne van Laatum, Roos Hogervorst, Carla Schep, and Frans J. Kok. "Malarial anemia leads to adequately increased erythropoiesis in asymptomatic Kenyan children." Blood 100, no. 10 (November 15, 2002): 3489–94. http://dx.doi.org/10.1182/blood-2001-12-0228.

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Malarial anemia is associated with a shift in iron distribution from functional to storage compartments. This suggests a relative deficit in erythropoietin production or action similar to that observed in other infections. Our study in Kenyan children with asymptomatic malaria aimed at investigating whether malaria causes increased erythropoiesis, and whether the erythropoietic response appeared appropriate for the degree of resulting anemia. Longitudinal and baseline data were used from a trial with a 2 × 2 factorial design, in which 328 anemic Kenyan children were randomly assigned to receiv

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Autino, Beatrice, Yolanda Corbett, Francesco Castelli, and Donatella Taramelli. "PATHOGENESIS OF MALARIA IN TISSUES AND BLOOD." Mediterranean Journal of Hematology and Infectious Diseases 4, no. 1 (October 4, 2012): e2012061. http://dx.doi.org/10.4084/mjhid.2012.061.

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The clinical manifestations of severe malaria are several and occur in different anatomical sites. Both parasite- and host-related factors contribute to the pathogenicity of the severe forms of the disease. Cytoadherence of infected red blood cells to the vascular endothelium of different organs and rosetting are unique features of malaria parasites which are likely to contribute to the vascular damage and the consequent excessive inflammatory/immune response of the host. In addition to cerebral malaria or severe anaemia, which are quite common manifestation of severe malaria, clinical evidenc

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Sun, Guang, Wun-Ling Chang, Jie Li, Seth Mark Berney, Donald Kimpel, and Henri C. van der Heyde. "Inhibition of Platelet Adherence to Brain Microvasculature Protects against Severe Plasmodium berghei Malaria." Infection and Immunity 71, no. 11 (November 2003): 6553–61. http://dx.doi.org/10.1128/iai.71.11.6553-6561.2003.

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ABSTRACT Some patients with Plasmodium falciparum infections develop cerebral malaria, acute respiratory distress, and shock and ultimately die even though drug therapy has eliminated the parasite from the blood, suggesting that a systemic inflammatory response contributes to malarial pathogenesis. Plasmodium berghei-infected mice are a well-recognized model of severe malaria (experimental severe malaria [ESM]), and infected mice exhibit a systemic inflammatory response. Because platelets are proposed to contribute to ESM and other systemic inflammatory responses, we determined whether platele

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21

Buffet, Pierre A., Innocent Safeukui, Guillaume Deplaine, Valentine Brousse, Virginie Prendki, Marc Thellier, Gareth D. Turner, and Odile Mercereau-Puijalon. "The pathogenesis of Plasmodium falciparum malaria in humans: insights from splenic physiology." Blood 117, no. 2 (January 13, 2011): 381–92. http://dx.doi.org/10.1182/blood-2010-04-202911.

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AbstractClinical manifestations of Plasmodium falciparum infection are induced by the asexual stages of the parasite that develop inside red blood cells (RBCs). Because splenic microcirculatory beds filter out altered RBCs, the spleen can innately clear subpopulations of infected or uninfected RBC modified during falciparum malaria. The spleen appears more protective against severe manifestations of malaria in naïve than in immune subjects. The spleen-specific pitting function accounts for a large fraction of parasite clearance in artemisinin-treated patients. RBC loss contributes to malarial

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22

Kho, Steven, Gabriela Minigo, Benediktus Andries, Leo Leonardo, Pak Prayoga, Jeanne R. Poespoprodjo, Enny Kenangalem, et al. "Circulating Neutrophil Extracellular Traps and Neutrophil Activation Are Increased in Proportion to Disease Severity in Human Malaria." Journal of Infectious Diseases 219, no. 12 (November 19, 2018): 1994–2004. http://dx.doi.org/10.1093/infdis/jiy661.

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AbstractBackgroundNeutrophil activation results in Plasmodium parasite killing in vitro, but neutrophil products including neutrophil extracellular traps (NETs) mediate host organ damage and may contribute to severe malaria. The role of NETs in the pathogenesis of severe malaria has not been examined.MethodsIn Papua, Indonesia, we enrolled adults with symptomatic Plasmodium falciparum (n = 47 uncomplicated, n = 8 severe), Plasmodium vivax (n = 37), or Plasmodium malariae (n = 14) malaria; asymptomatic P falciparum (n = 19) or P vivax (n = 21) parasitemia; and healthy adults (n = 23) without pa

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23

Rogerson, Stephen J., Lars Hviid, Patrick E. Duffy, Rose FG Leke, and Diane W. Taylor. "Malaria in pregnancy: pathogenesis and immunity." Lancet Infectious Diseases 7, no. 2 (February 2007): 105–17. http://dx.doi.org/10.1016/s1473-3099(07)70022-1.

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Hora, Rachna, Payal Kapoor, Kirandeep Kaur Thind, and Prakash Chandra Mishra. "Cerebral malaria – clinical manifestations and pathogenesis." Metabolic Brain Disease 31, no. 2 (January 8, 2016): 225–37. http://dx.doi.org/10.1007/s11011-015-9787-5.

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25

Spence, Philip J., and Jean Langhorne. "T cell control of malaria pathogenesis." Current Opinion in Immunology 24, no. 4 (August 2012): 444–48. http://dx.doi.org/10.1016/j.coi.2012.05.003.

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26

Clark, I. A., W. B. Cowden, and K. A. Rockett. "The pathogenesis of human cerebral malaria." Parasitology Today 10, no. 11 (January 1994): 417–18. http://dx.doi.org/10.1016/0169-4758(94)90170-8.

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27

Mendis, K. N., and R. Carter. "Clinical disease and pathogenesis in malaria." Parasitology Today 11, no. 5 (May 1995): PTI1—PTI16. http://dx.doi.org/10.1016/0169-4758(95)80143-x.

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28

Olatunde, Adesola C., Douglas H. Cornwall, Marshall Roedel, and Tracey J. Lamb. "Mouse Models for Unravelling Immunology of Blood Stage Malaria." Vaccines 10, no. 9 (September 14, 2022): 1525. http://dx.doi.org/10.3390/vaccines10091525.

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Malaria comprises a spectrum of disease syndromes and the immune system is a major participant in malarial disease. This is particularly true in relation to the immune responses elicited against blood stages of Plasmodium-parasites that are responsible for the pathogenesis of infection. Mouse models of malaria are commonly used to dissect the immune mechanisms underlying disease. While no single mouse model of Plasmodium infection completely recapitulates all the features of malaria in humans, collectively the existing models are invaluable for defining the events that lead to the immunopathog

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McDevitt, Michael A., Jianlin Xie, Shanmugasundaram Ganapathy-Kanniappan, Jason Griffith, Aihua Liu, Courtney McDonald, Philip Thuma, et al. "A critical role for the host mediator macrophage migration inhibitory factor in the pathogenesis of malarial anemia." Journal of Experimental Medicine 203, no. 5 (April 24, 2006): 1185–96. http://dx.doi.org/10.1084/jem.20052398.

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The pathogenesis of malarial anemia is multifactorial, and the mechanisms responsible for its high mortality are poorly understood. Studies indicate that host mediators produced during malaria infection may suppress erythroid progenitor development (Miller, K.L., J.C. Schooley, K.L. Smith, B. Kullgren, L.J. Mahlmann, and P.H. Silverman. 1989. Exp. Hematol. 17:379–385; Yap, G.S., and M.M. Stevenson. 1991. Ann. NY Acad. Sci. 628:279–281). We describe an intrinsic role for macrophage migration inhibitory factor (MIF) in the development of the anemic complications and bone marrow suppression that

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O’Sullivan, Jamie M., Roger J. S. Preston, Niamh O’Regan, and James S. O’Donnell. "Emerging roles for hemostatic dysfunction in malaria pathogenesis." Blood 127, no. 19 (May 12, 2016): 2281–88. http://dx.doi.org/10.1182/blood-2015-11-636464.

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Abstract Severe Plasmodium falciparum malaria remains a leading cause of mortality, particularly in sub-Saharan Africa where it accounts for up to 1 million deaths per annum. In spite of the significant mortality and morbidity associated with cerebral malaria (CM), the molecular mechanisms involved in the pathophysiology of severe malaria remain surprisingly poorly understood. Previous studies have demonstrated that sequestration of P falciparum–infected erythrocytes within the microvasculature of the brain plays a key role in the development of CM. In addition, there is convincing evidence th

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Wynn, Aye Aye, and Ohnmar Myint. "Role of Immunopathology in Clinical Course of Malaria: A Review." Borneo Journal of Medical Sciences (BJMS) 12, no. 3 (September 28, 2018): 3–10. http://dx.doi.org/10.51200/bjms.v12i3.1158.

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Malaria is a major health problem in various parts of the world especially affecting the tropical countries. It affects the vital organs causing severe complicated malaria. Clinical syndromes like severe cerebral anaemia, coagulation abnormalities, respiratory distress and severe anaemia can increase the mortality of malaria infected cases. Variation in individual susceptibility and severity and type of clinical presentations of malaria raises the need for study of both the parasite and host immune reactions as well as the contribution of inflammatory cytokines in malaria pathogenesis. This st

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ROGERSON, S. J., and P. BOEUF. "New approaches to pathogenesis of malaria in pregnancy." Parasitology 134, no. 13 (October 25, 2007): 1883–93. http://dx.doi.org/10.1017/s003118200700011x.

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SUMMARYMalaria infection during pregnancy is associated with poor maternal and foetal outcomes including low birth weight. In malaria-endemic areas, low birth weight is primarily a consequence of foetal growth restriction. Little is known on the pathogenesis of foetal growth restriction and our understanding of the relationship between epidemiological observations and the pathogenesis or consequences of disease is incomplete. In this review, we describe these gaps in our knowledge and also try to identify goals for future research into malaria in pregnancy. Foetal growth restriction results fr

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Nussenblatt, Veronique, Gelasius Mukasa, Amy Metzger, Grace Ndeezi, Elizabeth Garrett, and Richard D. Semba. "Anemia and Interleukin-10, Tumor Necrosis Factor Alpha, and Erythropoietin Levels among Children with Acute, Uncomplicated Plasmodium falciparum Malaria." Clinical Diagnostic Laboratory Immunology 8, no. 6 (November 1, 2001): 1164–70. http://dx.doi.org/10.1128/cdli.8.6.1164-1170.2001.

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ABSTRACT Anemia is an important complication of malaria, and its pathogenesis is not well understood. To gain insight into potential age-related relationships between tumor necrosis factor alpha (TNF-α), interleukin 10 (IL-10), erythropoietin, and anemia during acute malaria, 273 children of ages 12 to 120 months presenting with acute, uncomplicated malaria in Kampala, Uganda, were monitored at enrollment and 3 and 7 days later. Younger children had higher geometric mean erythropoietin, TNF-α, and α1-acid glycoprotein (AGP) concentrations than older children. Univariate regression analysis rev

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Lamb, Tracey J., Douglas E. Brown, Alexandre J. Potocnik, and Jean Langhorne. "Insights into the immunopathogenesis of malaria using mouse models." Expert Reviews in Molecular Medicine 8, no. 6 (March 23, 2006): 1–22. http://dx.doi.org/10.1017/s1462399406010581.

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Malaria kills approximately 1–2 million people every year, mostly in sub-Saharan Africa and in Asia. These deaths are at the most severe end of a scale of pathologies affecting approximately 500 million people per year. Much of the pathogenesis of malaria is caused by inappropriate or excessive immune responses mounted by the body to eliminate malaria parasites. In this review, we examine the evidence that immunopathology is responsible for malaria disease in the context of what we have learnt from animal models of malaria. In particular, we look in detail at the processes involved in endothel

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35

Clark, Ian A., Lisa M. Alleva, Alison C. Mills, and William B. Cowden. "Pathogenesis of Malaria and Clinically Similar Conditions." Clinical Microbiology Reviews 17, no. 3 (July 2004): 509–39. http://dx.doi.org/10.1128/cmr.17.3.509-539.2004.

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SUMMARY There is now wide acceptance of the concept that the similarity between many acute infectious diseases, be they viral, bacterial, or parasitic in origin, is caused by the overproduction of inflammatory cytokines initiated when the organism interacts with the innate immune system. This is also true of certain noninfectious states, such as the tissue injury syndromes. This review discusses the historical origins of these ideas, which began with tumor necrosis factor (TNF) and spread from their origins in malaria research to other fields. As well the more established proinflammatory media

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Lawton, Jonathan G., Albert E. Zhou, Drissa Coulibaly, Emily M. Stucke, Antoine Dara, Matthew B. Laurens, Joana C. Silva, Mahamadou A. Thera, and Mark A. Travassos. "272 Differential expression of two Plasmodium falciparum variant surface antigen families in Malian children with cerebral malaria compared to mild malaria." Journal of Clinical and Translational Science 7, s1 (April 2023): 81–82. http://dx.doi.org/10.1017/cts.2023.330.

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OBJECTIVES/GOALS: Recent in vitro evidence suggests that diverse parasite protein families called RIFINs and STEVORs are displayed on the surface of infected red blood cells and may have a role in severe malaria, but they remain sparsely studied in natural infections. We measured the RNA expression of these antigens in Malian children with severe or mild malaria illness. METHODS/STUDY POPULATION: We collected blood samples from Malian children aged six months to five years, including 14 with cerebral malaria, 10 with severe malarial anemia, and demographic-matched controls with mild, uncomplic

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Aprilen, Nisa, and I. Made Bayu Indratama. "Handling cerebral malaria patient with limited resources: a case report." Jurnal Penyakit Dalam Udayana 5, no. 2 (December 20, 2021): 26–31. http://dx.doi.org/10.36216/jpd.v5i2.149.

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Cerebral malaria is an emergency condition. All patients with Plasmodium falciparum infection followed by neurological symptoms should be treated as cerebral malaria. The pathogenesis of cerebral malaria is caused by the damage of blood vessels endothelium due to parasites sequestration, production of pro-inflammatory cytokines and leakage of blood vessels which can cause brain hypoxia. The proper management is needed, however this become quiet challenging issue in the setting of limited resouces. We report a case of a 35 year old patient presenting with a loss of consciousness accompanied by

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Mawson, Anthony R. "The pathogenesis of malaria: a new perspective." Pathogens and Global Health 107, no. 3 (April 2013): 122–29. http://dx.doi.org/10.1179/2047773213y.0000000084.

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Pati, Sudhanshu S., and Saroj K. Mishra. "Pathogenesis of cerebral malaria—a step forward." Nature Reviews Neurology 8, no. 8 (July 24, 2012): 415–16. http://dx.doi.org/10.1038/nrneurol.2012.144.

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Mackintosh, Claire L., James G. Beeson, and Kevin Marsh. "Clinical features and pathogenesis of severe malaria." Trends in Parasitology 20, no. 12 (December 2004): 597–603. http://dx.doi.org/10.1016/j.pt.2004.09.006.

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Hempel, Casper, Erica M. Pasini, and Jørgen A. L. Kurtzhals. "Endothelial Glycocalyx: Shedding Light on Malaria Pathogenesis." Trends in Molecular Medicine 22, no. 6 (June 2016): 453–57. http://dx.doi.org/10.1016/j.molmed.2016.04.004.

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Matar, C. G., N. T. Jacobs, S. H. Speck, T. J. Lamb, and A. M. Moormann. "Does EBV alter the pathogenesis of malaria?" Parasite Immunology 37, no. 9 (September 2015): 433–45. http://dx.doi.org/10.1111/pim.12212.

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Akanmori, Bartholomew D. "Malaria Immunology and Pathogenesis Consortium (MIMPAC) formed." Trends in Parasitology 17, no. 5 (May 2001): 215. http://dx.doi.org/10.1016/s1471-4922(01)01962-6.

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Maung Oo, Maung, and Than Than. "Pathogenesis of ring-haemorrhage in cerebral malaria." Annals of Tropical Medicine & Parasitology 83, no. 5 (January 1989): 555–57. http://dx.doi.org/10.1080/00034983.1989.11812387.

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Chin, Voon Kin, Chong WC, Haniza H, and Rusliza Basir. "MODULATING EFFECTS OF IL-4, IL-10 AND IL-13 ON THE COURSE OF PLASMODIUM BERGHEI MALARIA INFECTION IN MICE." Journal of Health and Translational Medicine 24, no. 2 (September 24, 2021): 92–105. http://dx.doi.org/10.22452/jummec.vol24no2.13.

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Background: Inflammation is a crucial process driving pathogenesis in malaria infection. The devastating effects of malaria infection has always been associated with severe inflammation whilst protective effect is linked to provocation of anti-inflammation responses. IL-4, IL-10 and IL-13 are well-established anti-inflammatory cytokines with their functional roles during malaria infection remain elusive. Therefore, this study was undertaken to study the effects of modulating IL-10, IL-4 and IL-13 on the course of malaria infection in Plasmodium berghei ANKA (PbA)-infected murine model. Methods

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Guenther, Geoffrey, Alexuse M. Saidi, Rima Izem, Karl Seydel, and Douglas G. Postels. "Post-Malaria Anemia Is Rare in Malawian Children with Cerebral Malaria." American Journal of Tropical Medicine and Hygiene 104, no. 6 (June 2, 2021): 2146–51. http://dx.doi.org/10.4269/ajtmh.20-1668.

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Abstract.Artesunate therapy for severe malaria syndromes has been associated with post-treatment hemolysis and anemia. We defined post-malaria anemia as any decrease in hematocrit between the index hospitalization for severe malaria and 1 month after. We determined the incidence and severity of post-malaria anemia in Malawian children surviving cerebral malaria (CM) by analyzing hospital and follow-up data from a long-standing study of CM pathogenesis. Children enrolled before 2014 and treated with quinine (N = 258) were compared with those admitted in 2014 and after, and treated with artesuna

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Hawkes, Michael T., Aleksandra Leligdowicz, Anthony Batte, Geoffrey Situma, Kathleen Zhong, Sophie Namasopo, Robert O. Opoka, Kevin C. Kain, and Andrea L. Conroy. "Pathophysiology of Acute Kidney Injury in Malaria and Non-Malarial Febrile Illness: A Prospective Cohort Study." Pathogens 11, no. 4 (April 3, 2022): 436. http://dx.doi.org/10.3390/pathogens11040436.

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Acute kidney injury (AKI) is a life-threatening complication. Malaria and sepsis are leading causes of AKI in low-and-middle-income countries, but its etiology and pathogenesis are poorly understood. A prospective observational cohort study was conducted to evaluate pathways of immune and endothelial activation in children hospitalized with an acute febrile illness in Uganda. The relationship between clinical outcome and AKI, defined using the Kidney Disease: Improving Global Outcomes criteria, was investigated. The study included 967 participants (mean age 1.67 years, 44.7% female) with 687 (

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NEBL, T., M. J. DE VEER, and L. SCHOFIELD. "Stimulation of innate immune responses by malarial glycosylphosphatidylinositol via pattern recognition receptors." Parasitology 130, S1 (March 2005): S45—S62. http://dx.doi.org/10.1017/s0031182005008152.

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The glycosylphosphatidylinositol (GPI) anchor ofPlasmodium falciparumis thought to function as a critical toxin that contributes to severe malarial pathogenesis by eliciting the production of proinflammatory responses by the innate immune system of mammalian hosts. Analysis of the fine structure ofP. falciparumGPI suggests a requirement for the presence of both core glycan and lipid moieties in the recognition and signalling of parasite glycolipids by host immune cells. It has been demonstrated that GPI anchors of various parasitic protozoa can mediate cellular immune responses via members of

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Wande, I. Nyoman, Endang Retnowati, and Juli Soemarsono. "KADAR INTERLEUKIN 10 (IL-10) MALARIA DAN ANEMIA." INDONESIAN JOURNAL OF CLINICAL PATHOLOGY AND MEDICAL LABORATORY 18, no. 1 (October 14, 2016): 4. http://dx.doi.org/10.24293/ijcpml.v18i1.767.

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Anaemia is an important complication of malaria, and its pathogenesis is not well understood. High level of the Th2 cytokine (such as IL-10), which counteract the Th1 cytokine, might prevent the development of severe malarial anaemia. The purpose of this study was to know the comparation between the plasma level of IL-10 in malaria patients with anaemia and without anaemia. The plasma level of IL-10 was examined in 16 malaria patients with anaemia and 16 malaria caused by P. falciparum patients without anaemia samplestaken from patients at the primary health centres in West Lombok and Centre L

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Knackstedt, Sebastian Lorenz, Athina Georgiadou, Falko Apel, Ulrike Abu-Abed, Christopher A. Moxon, Aubrey J. Cunnington, Bärbel Raupach, et al. "Neutrophil extracellular traps drive inflammatory pathogenesis in malaria." Science Immunology 4, no. 40 (October 18, 2019): eaaw0336. http://dx.doi.org/10.1126/sciimmunol.aaw0336.

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Neutrophils are essential innate immune cells that extrude chromatin in the form of neutrophil extracellular traps (NETs) when they die. This form of cell death has potent immunostimulatory activity. We show that heme-induced NETs are essential for malaria pathogenesis. Using patient samples and a mouse model, we define two mechanisms of NET-mediated inflammation of the vasculature: activation of emergency granulopoiesis via granulocyte colony-stimulating factor production and induction of the endothelial cytoadhesion receptor intercellular adhesion molecule–1. Soluble NET components facilitat

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