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  1. Medical Microbiology and Immunology
  2. Medical Microbiology and Immunology : Volume 201
  3. Medical Microbiology and Immunology : Volume 201, Issue 4, November 2012
  4. Pathogenesis of malaria revisited
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Medical Microbiology and Immunology : Volume 205
Medical Microbiology and Immunology : Volume 204
Medical Microbiology and Immunology : Volume 203
Medical Microbiology and Immunology : Volume 202
Medical Microbiology and Immunology : Volume 201
Medical Microbiology and Immunology : Volume 201, Issue 4, November 2012
Mechanisms of invasion and persistence of infectious agents
Modulation of translation and induction of autophagy by bacterial exoproducts
Pore-forming bacterial toxins and antimicrobial peptides as modulators of ADAM function
Principles of polyoma- and papillomavirus uncoating
Host-cell factors involved in papillomavirus entry
Host factors involved in hepatitis B virus maturation, assembly, and egress
Census of cytosolic aminopeptidase activity reveals two novel cytosolic aminopeptidases
Live or let die: manipulation of cellular suicide programs by murine cytomegalovirus
Innate immunity regulates adaptive immune response: lessons learned from studying the interplay between NK and CD8+ T cells during MCMV infection
Murine cytomegalovirus immune evasion proteins operative in the MHC class I pathway of antigen processing and presentation: state of knowledge, revisions, and questions
Antigen presentation under the influence of ‘immune evasion’ proteins and its modulation by interferon-gamma: implications for immunotherapy of cytomegalovirus infection with antiviral CD8 T cells
Parameters determining the efficacy of adoptive CD8 T-cell therapy of cytomegalovirus infection
Immune control in the absence of immunodominant epitopes: implications for immunotherapy of cytomegalovirus infection with antiviral CD8 T cells
Viral latency drives ‘memory inflation’: a unifying hypothesis linking two hallmarks of cytomegalovirus infection
Nucleocytoplasmic shuttling and CRM1-dependent MHC class I peptide presentation of human cytomegalovirus pp65
Dendritic cells in Leishmania major infections: mechanisms of parasite uptake, cell activation and evidence for physiological relevance
Malaria and human red blood cells
Pathogenesis of malaria revisited
Medical Microbiology and Immunology : Volume 201, Issue 3, August 2012
Medical Microbiology and Immunology : Volume 201, Issue 2, May 2012
Medical Microbiology and Immunology : Volume 201, Issue 1, February 2012
Medical Microbiology and Immunology : Volume 200
Medical Microbiology and Immunology : Volume 199
Medical Microbiology and Immunology : Volume 198
Medical Microbiology and Immunology : Volume 197
Medical Microbiology and Immunology : Volume 196
Medical Microbiology and Immunology : Volume 195
Medical Microbiology and Immunology : Volume 194
Medical Microbiology and Immunology : Volume 193
Medical Microbiology and Immunology : Volume 192
Medical Microbiology and Immunology : Volume 191
Medical Microbiology and Immunology : Volume 190
Medical Microbiology and Immunology : Volume 189
Medical Microbiology and Immunology : Volume 188
Medical Microbiology and Immunology : Volume 187
Medical Microbiology and Immunology : Volume 186
Medical Microbiology and Immunology : Volume 185

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Pathogenesis of malaria revisited

Content Provider Springer Nature Link
Author Dasari, Prasad Bhakdi, Sucharit
Copyright Year 2012
Abstract Plasmodium falciparum malaria claims 1 million lives around the globe every year. Parasitemia can reach remarkably high levels. The developing parasite digests hemoglobin and converts the waste product to hemozoin alias malaria pigment. These processes occur in a vesicular compartment named the digestive vacuole (DV). Each parasitized cell releases one DV upon rupture. Myriads of DVs thus gain entry into the blood, but whether they trigger pathobiological events has never been investigated. We recently discovered that the DV membrane simultaneously activates the two major enzyme cascades in blood, complement and coagulation. Activation of both is known to occur in patients with severe malaria, so discovery of the common trigger has large consequences. The DV membrane but not the merozoite has the capacity to spontaneously activate the alternative complement and intrinsic clotting pathway. Ejection of merozoites and the DV into the bloodstream, therefore, results in selective opsonization and phagocytosis of the DV, leaving merozoites free to invade new cells. The DV membrane furthermore has the capacity to assemble prothrombinase, the key convertase of the intrinsic clotting pathway. The dual capacity of the DV to activate both complement and coagulation can be suppressed by low-molecular-weight dextran sulfate. This agent protects experimental animals from the detrimental consequences, resulting from intravenous application of purified DVs. Phagocytosis of DVs not only deploys PMN away from merozoites, but also drives the cells into a state of functional exhaustion. This may be one reason for the enhanced susceptibility of patients with severe malaria toward systemic bacterial infections. Together, these findings indicate that the DV may represent a hitherto unrecognized, important determinant of parasite pathogenicity.
Starting Page 599
Ending Page 604
Page Count 6
File Format PDF
ISSN 03008584
Journal Medical Microbiology and Immunology
Volume Number 201
Issue Number 4
e-ISSN 14321831
Language English
Publisher Springer-Verlag
Publisher Date 2012-09-07
Publisher Place Berlin/Heidelberg
Access Restriction One Nation One Subscription (ONOS)
Subject Keyword Malaria Digestive vacuole Complement Coagulation Immunopathogenesis Medical Microbiology Immunology
Content Type Text
Resource Type Article
Subject Immunology and Allergy Immunology Microbiology (medical)
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