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Journal articles on the topic 'Malaria – Pathogenesis'

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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 polymorphism (RFLP). Compared with healthy controls, heterozygosity protected against clinical malaria: uncomplicated malaria (odds ratios [OR] = 0.13, P < 0.001), severe malarial anemia (OR = 0.18, P < 0.001), and cerebral malaria (OR = 0.39, P = 0.022). Levels of total IgE significantly differed among malaria phenotypes (P = 0.044) and rs3024974 genotypes (P = 0.037). Neither cytokine levels nor IL-6/IL-10 ratios were associated with malaria phenotypes or rs3024974 genotypes. This study suggests a role for rs3024974 in malaria pathogenesis and offers further insights into an IL-4/STAT6 pathway mutation in malaria pathogenesis.
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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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7

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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10

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 falciparum.
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11

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 children presenting with cerebral malaria (median lymphocyte count, 2,100/μl) and uncomplicated malaria (3,700/μl), which was corrected in convalescence and was absent in severe malarial anemia (5,950/μl). Median percentages of activated CD69+NK (73%) and γδ T (60%) cells were higher in cerebral malaria than in other malaria types. Median ratios of memory to naive CD4+lymphocytes were higher in cerebral malaria than in uncomplicated malaria and low in severe malarial anemia. The polarized lymphocyte subset profiles of different forms of severe malaria are independent of age. In conclusion, among Malawian children cerebral malaria is characterized by lymphocyte activation and increased memory cells, consistent with immune priming. In contrast, there are reduced memory cells and less activation in severe malaria anemia. Further studies are required to understand whether these immunological profiles indicate predisposition of some children to one or another form of severe malaria.
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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 mice. P-selectin levels assessed by the quantitative dual radiolabeled monoclonal antibody technique increased significantly (P < 0.05) in several organs in C57BL/6 mice infected with P. berghei, supporting the concept of a systemic inflammatory response mediating malarial pathogenesis. Intravital microscopic analysis of the brain microvasculature demonstrated significant (P < 0.001) leukocyte rolling and adhesion in brain venules of P. berghei-infected mice compared with those found in uninfected controls. The maximum leukocyte adhesion occurred on day 6 of P. berghei infection, when the mice become moribund and exhibit marked vascular leakage into the brain, lung, and heart. However, P-selectin levels were significantly (P < 0.005) increased in brain, lung, and kidneys during P. berghei malaria in ECM-resistant BALB/c mice compared with those found in uninfected BALB/c controls, indicating that increased P-selectin alone is not sufficient to mediate malarial pathogenesis. Leukocyte adhesion to brain microvessels of P-selectin-deficient mice with P. berghei malaria was similar to that observed in control mice. Collectively, these results indicate that P-selectin is important for the development of malarial pathogenesis but is not required for leukocyte adhesion in brain.
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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 proteins are encoded by a large and extremely diverse family of genes (var), and switches in the expression of var genes account for rapid changes in the antigenic and adhesive properties of P. falciparum-inkcted erythrocytes (2.4% per generation). Switches in the PfEMPl expression may not only affect the phenotype of the parasite strain but may also change its sequestration to endothelial cells. Genetic reorganization in this protein can lead to binding any of the following endothelial cell receptors; ICAM-1, CD36, thrombospondin, chondroitin sulfate (Fig. 5),2 ELAM-1, or VCAM-1.
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15

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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17

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 receive either iron or placebo, and sulfadoxine-pyrimethamine or placebo. Erythropoiesis was evaluated by serum concentrations of erythropoietin and soluble transferrin receptor. Prospectively collected data showed that malarial infection resulted in decreased hemoglobin concentrations, and increased serum concentrations of erythropoietin and transferrin receptor. Conversely, disappearance of malarial antigenemia resulted in increased hemoglobin concentrations, and decreased concentrations of these serum indicators. Additionally, our baseline data showed that current or recent malarial infection is associated with increased serum concentrations of erythropoietin and transferrin receptor, and that these were as high as or perhaps even higher than values of children without malarial infection and without inflammation. Our findings indicate that in asymptomatic malaria, the erythropoietic response is adequate for the degree of anemia, and that inflammation probably plays no or only a minor role in the pathogenesis of the resulting anemia. Further research is needed to demonstrate the role of deficient erythropoietin production or action in the pathogenesis of the anemia of symptomatic malaria.
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19

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 evidences of thrombocytopenia, acute respiratory distress syndrome (ARDS), liver and kidney disease, are reported. In primigravidae from endemic areas, life threatening placental malaria may also be present.In the following pages, some of the pathogenetic aspects will be briefly reviewed and then data on selected and less frequent manifestation of severe malaria, such as liver or renal failure or ARDS will be discussed
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20

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 platelet adherence contributes to experimental malarial pathogenesis. Indeed, a significant (P < 0.005) increase in the number of rolling and adherent platelets was observed by intravital microscopy in brain venules of P. berghei-infected mice compared with the number in uninfected controls. P-selectin- or ICAM-1-deficient mice exhibit increased survival after P. berghei infection. We observed a significant (P < 0.0001) reduction in the morbidity of mice injected with anti-CD41 (αIIb or gpIIb) monoclonal antibody on day 1 of P. berghei infection compared with the morbidity of infected controls injected with rat immunoglobulin G. Additionally, platelet rolling and adhesion in brain venules were reduced in P. berghei mice lacking either P-selectin or ICAM-1 or when the platelets were coated with anti-CD41 monoclonal antibody. Unlike other inflammatory conditions, we did not detect platelet-leukocyte interactions during P. berghei malaria. Because (i) leukocyte adhesion is not markedly altered in the absence of P-selectin or ICAM-1 and (ii) CD41 is not an adhesion molecule for parasitized erythrocytes, these findings support the hypothesis that inhibition of platelet adhesion to the brain microvasculature protects against development of malarial pathogenesis.
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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 anemia, a clinical form associated with subacute progression, frequent splenomegaly, and relatively low parasitemia. Stringent splenic clearance of ring-infected RBCs and uninfected, but parasite-altered, RBCs, may altogether exacerbate anemia and reduce the risks of severe complications associated with high parasite loads, such as cerebral malaria. The age of the patient directly influences the risk of severe manifestations. We hypothesize that coevolution resulting in increased splenic clearance of P. falciparum–altered RBCs in children favors the survival of the host and, ultimately, sustained parasite transmission. This analysis of the RBC–spleen dynamic interactions during P falciparum infection reflects both data and hypotheses, and provides a framework on which a more complete immunologic understanding of malaria pathogenesis may be elaborated.
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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 parasitemia. Neutrophil activation and NETs were quantified by immunoassays and microscopy and correlated with parasite biomass and disease severity.ResultsIn patients with symptomatic malaria, neutrophil activation and NET counts were increased in all 3 Plasmodium species. In falciparum malaria, neutrophil activation and NET counts positively correlated with parasite biomass (Spearman rho = 0.41, P = .005 and r2 = 0.26, P = .002, respectively) and were significantly increased in severe disease. In contrast, NETs were inversely associated with parasitemia in adults with asymptomatic P falciparum infection (r2 = 0.24, P = .031) but not asymptomatic P vivax infection.ConclusionsAlthough NETs may inhibit parasite growth in asymptomatic P falciparum infection, neutrophil activation and NET release may contribute to pathogenesis in severe falciparum malaria. Agents with potential to attenuate these processes should be evaluated.
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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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24

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 immunopathogenesis of malaria. Here we review the different mouse models of Plasmodium infection that are available, and highlight some of the main contributions these models have made with regards to identifying immune mechanisms of parasite control and the immunopathogenesis of malaria.
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29

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 are associated with malaria infection. At concentrations found in the circulation of malaria-infected patients, MIF suppressed erythropoietin-dependent erythroid colony formation. MIF synergized with tumor necrosis factor and γ interferon, which are known antagonists of hematopoiesis, even when these cytokines were present in subinhibitory concentrations. MIF inhibited erythroid differentiation and hemoglobin production, and it antagonized the pattern of mitogen-activated protein kinase phosphorylation that normally occurs during erythroid progenitor differentiation. Infection of MIF knockout mice with Plasmodium chabaudi resulted in less severe anemia, improved erythroid progenitor development, and increased survival compared with wild-type controls. We also found that human mononuclear cells carrying highly expressed MIF alleles produced more MIF when stimulated with the malarial product hemozoin compared with cells carrying low expression MIF alleles. These data suggest that polymorphisms at the MIF locus may influence the levels of MIF produced in the innate response to malaria infection and the likelihood of anemic complications.
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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 that both endothelial cell activation and platelets play critical roles in the modulating the pathogenesis of severe P falciparum malaria. In this review, we provide an overview of recent studies that have identified novel roles through which hemostatic dysfunction may directly influence malaria pathogenesis. In particular, we focus on emerging data suggesting that von Willebrand factor, coagulation cascade activation, and dysfunction of the protein C pathway may be of specific importance in this context. These collective insights underscore a growing appreciation of the important, but poorly understood, role of hemostatic dysfunction in malaria progression and, importantly, illuminate potential approaches for novel therapeutic strategies. Given that the mortality rate associated with CM remains on the order of 20% despite the availability of effective antimalarial therapy, development of adjunctive therapies that can attenuate CM progression clearly represents a major unmet need. These emerging data are thus not only of basic scientific interest, but also of direct clinical significance.
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31

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 study explored the immunopathological basis and advances of severe malaria and their importance in pathogenesis of malaria and its complications. Previous and ongoing studies indicate that changes in endothelium during the sequestration of parasites in organs causes disruption of endothelial barrier function leading to serious effects of malaria. Parasite and host factors contribute to disturbance of cytokine regulation and escape of parasites from the immune system of the host. Immunopathological changes and dysregulation of cytokine production play central role in pathogenesis and disease severity in malaria.
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32

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 from a complex four-dimensional interaction between the foetus, the mother and the malaria parasite over gestation, and research into its pathogenesis may be advanced by combining longitudinal studies with techniques and approaches new to the field of malaria in pregnancy. Such approaches would greatly increase our knowledge on the pathogenesis of this disease and may provide new avenues for intervention strategies.
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33

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 revealed that age, log10 erythropoietin levels, IL-10/TNF-α ratio, and AGP levels were each significantly associated with hemoglobin levels at baseline. Hemoglobin concentrations were inversely correlated with the log10erythropoietin level at all three visits. For the older age groups, higher levels of TNF-α were significantly associated with higher IL-10 levels at all three visits, but this relationship was significant only at baseline for younger children. These data suggest that younger children do not maintain IL-10 production in response to the inflammatory process, and this mechanism may contribute to the more severe anemia found in younger children. Acute malaria is an illness whose incidence and severity are largely age dependent. Further studies are needed to understand the relationships between age-related immune responses to malaria and their role in the pathogenesis of malarial anemia.
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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 endothelial cell damage leading to syndromes such as cerebral malaria, as well as generalised systemic manifestations such as anaemia, cachexia and problems with thermoregulation of the body. We also consider malaria in light of the variation of the severity of disease observed among people, and discuss the contribution from animal models to our understanding of this variation. Finally, we discuss some of the implications of immunopathology, and of host and parasite genetic variation, for the design and implementation of anti-malarial vaccines.
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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 mediators, such as TNF, interleukin-1, and lymphotoxin, the roles of nitric oxide and carbon monoxide, which are chiefly inhibitory, are discussed. The established and potential roles of two more recently recognized contributors, overactivity of the enzyme poly(ADP-ribose) polymerase 1 (PARP-1) and the escape of high-mobility-group box 1 (HMGB1) protein from its normal location into the circulation, are also put in context. The pathogenesis of the disease caused by falciparum malaria is then considered in the light of what has been learned about the roles of these mediators in these other diseases, as well as in malaria itself.
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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, uncomplicated malaria. We extracted total RNA from each patient and used a custom capture array to selectively enrich Plasmodium falciparum parasite RNA. We then performed Illumina next-generation RNA sequencing and reconstructed parasite transcriptomes using reference-free de novo assembly. We identified RNA encoding RIFINs and STEVORs using an in-house classifier, then measured the diversity and abundance of gene expression for each infection. Expression diversity was defined as the number of unique variants transcribed. Expression abundance was calculated as transcripts per million (TPM). RESULTS/ANTICIPATED RESULTS: Cerebral malaria cases, but not severe malarial anemia cases, had higher diversity and abundance of RIFIN expression compared to mild infections. Type A RIFINs predominated over Type B RIFINs, and the same two RIFINs were predominantly expressed in all disease phenotypes. We anticipate that predominantly expressed RIFINs share high sequence homology with variants previously shown to bind blood antigens or immune inhibitory receptors. STEVOR expression was also higher in cerebral malaria compared to mild malaria, but STEVOR transcripts were sparse overall. DISCUSSION/SIGNIFICANCE: Elevated RIFIN expression in cerebral malaria over mild malaria supports a role for these antigens in pathogenesis. Severe malarial anemia may progress through a different pathogenic mechanism. Predominantly expressed RIFIN variants may be promising targets for vaccines and therapeutics to protect children against cerebral malaria.
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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 shivering fever for 5 days. On examination of the peripheral blood smear, the Plasmodium falciparum was found. The patient was later diagnosed as cerebral malaria and treated with anti-malarial drugs. The fifth day of treatment the patient has fully alert. In the next day, the patient was allowed to go home. The management of cerebral malaria is challenging, particularly in the area with limited resources.
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38

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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39

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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41

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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42

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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43

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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44

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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45

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: Male ICR mice were randomly assigned into 5 different groupings and were infected intraperitoneal with 0.2 mL of 2 x 107 pRBCs containing P. berghei ANKA (PbA). Malaria-infected mice were treated with recombinant mouse IL-4 (rmIL-4), recombinant mouse IL-10 (rmIL-10) and recombinant mouse IL-13 (rmIL-13) for 4 consecutive days after the establishment of the infection. The survival and parasitemia levels of malarial mice and malarial mice under different treatments were monitored. Major affected organs (kidneys, lungs, brain, liver and spleen) were subjected to histopathological analysis at day-5 post infection. Results: Our findings revealed that the overall lifespan of malarial mice treated with recombinant mouse rmIL10, rmIL-4 and rmIL-13 were prolonged, accompanied with significant reduction in malaria parasitemia levels, in particular in malarial mice receiving recombinant rmIL-10 and rmIL-13. Histopathological conditions of kidneys, lungs, brain, liver and spleen treated with recombinant mouse rmIL-10, rmIL-4 and rmIL-13 were also improved. Sequestration of parasitized red blood cells (pRBCs) and inflammation seen in major affected organs were alleviated. Conclusion: Despite some limitations, this preliminary study demonstrated the promising therapeutic effects of IL-10 and IL-13 as adjuvant therapies in reducing severe pathological manifestations triggered by inflammation during malaria infection.
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46

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 artesunate (N = 235). The last hematocrit value obtained during hospitalization was compared with the 1-month post-hospitalization hematocrit value. The overall rate of a post-hospitalization decrease in hematocrit in children surviving CM was 5.3% (11 of 235 or 4.7% for quinine, 15 of 258 or 5.8% for artesunate; odds ratio, 3.23 [0.88, 18.38]); no patients with a decrease in hematocrit were symptomatic, and none required transfusion after hospitalization. Of the 26 children who had a decrease in hematocrit 1 month after hospitalization, 23.1% had evidence of a new malaria infection. When children treated with quinine and artesunate were combined, a higher hematocrit level on admission, lower quantitative histidine-rich protein level, and splenomegaly were associated independently with post-malaria anemia. In African survivors of CM, post-malaria anemia is rare, mild, and unassociated with the anti-malarial treatment received.
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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 (71.0%) positive for malaria by rapid diagnostic test and 280 (29.1%) children had a non-malarial febrile illness (NMFI). The frequency of AKI was higher in children with NMFI compared to malaria (AKI, 55.0% vs. 46.7%, p = 0.02). However, the frequency of severe AKI (stage 2 or 3 AKI) was comparable (12.1% vs. 10.5%, p = 0.45). Circulating markers of both immune and endothelial activation were associated with severe AKI. Children who had malaria and AKI had increased mortality (no AKI, 0.8% vs. AKI, 4.1%, p = 0.005), while there was no difference in mortality among children with NMFI (no AKI, 4.0% vs. AKI, 4.6%, p = 0.81). AKI is a common complication in children hospitalized with acute infections. Immune and endothelial activation appear to play central roles in the pathogenesis of AKI.
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48

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 the Toll-like family of pattern recognition receptors (TLRs). Recent studies indicate that GPI anchors ofP. falciparumand other protozoa are preferentially recognized by TLR-2, involving the MyD88-dependent activation of specific signalling pathways that mediate the production of proinflammatory cytokines and nitric oxide from host macrophagesin vitro. However, the contribution of malaria GPI toxin to severe disease syndromes and the role of specific TLRs or other pattern recognition receptors in innate immunityin vivois only just beginning to be characterized. A better understanding of the molecular mechanisms underlying severe malarial pathogenesis may yet lead to substantial new insights with important implications for the development of novel therapeutics for malaria treatment.
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49

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 Lombok during March until July 2008. The samples were measured using ELISA. The concentration of haemoglobin (Hb) was measured using hematological analyzer. The anaemia concentration of Hb is <11 g/dL. The results were analyzed using two (2) sample t test with SPSS ver.13.The plasma level of IL-10 in malaria patients caused by P. falciparum with anaemia was 8.81(3.04) [mean(SD)] pg/mL where as the plasma level of IL-10 in malaria patients without anaemia was 47.99(25.26) pg/mL. The mean of IL-10 level in malaria falciparum patients with anaemia was significantly lower than that of malaria patients caused by P. falciparum without anaemia (p=0.000).
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50

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 facilitate parasite sequestration and mediate tissue destruction. We demonstrate that neutrophils have a key role in malaria immunopathology and propose inhibition of NETs as a treatment strategy in vascular infections.
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