Article

Fatal Plasmodium falciparum malaria causes specific patterns of splenic architectural disorganization.

Centre for Clinical Vaccinology and Tropical Medicine, Churchill Hospital, University of Oxford, Old Road, Oxford, OX3 7LJ, United Kingdom.
Infection and Immunity (impact factor: 4.16). 05/2005; 73(4):1986-94. DOI:10.1128/IAI.73.4.1986-1994.2005 pp.1986-94
Source: PubMed

ABSTRACT The spleen is critical for host defense against pathogens, including Plasmodium falciparum. It has a dual role, not only removing aged or antigenically altered erythrocytes from the blood but also as the major lymphoid organ for blood-borne or systemic infections. The human malaria parasite P. falciparum replicates within erythrocytes during asexual blood stages and causes repeated infections that can be associated with severe disease. In spite of the crucial role of the spleen in the innate and acquired immune response to malaria, there is little information on the pathology of the spleen in human malaria. We performed a histological and quantitative immunohistochemical study of spleen sections from Vietnamese adults dying from severe falciparum malaria and compared the findings with the findings for spleen sections from control patients and patients dying from systemic bacterial sepsis. Here we report that the white pulp in the spleens of patients dying from malaria showed a marked architectural disorganization. We observed a marked dissolution of the marginal zones with relative loss of B cells. Furthermore, we found strong HLA-DR expression on sinusoidal lining cells but downregulation on cordal macrophages. P. falciparum infection results in alterations in splenic leukocytes, many of which are not seen in sepsis.

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Keywords

asexual blood stages
 
B cells
 
cordal macrophages
 
crucial role
 
dual role
 
host defense
 
major lymphoid organ
 
marked architectural disorganization
 
marked dissolution
 
P. falciparum infection results
 
Plasmodium falciparum
 
quantitative immunohistochemical study
 
relative loss
 
severe disease
 
severe falciparum malaria
 
spleens
 
splenic leukocytes
 
strong HLA-DR expression
 
systemic bacterial sepsis
 
systemic infections