Evidence of endothelial inflammation, T cell activation, and T cell reallocation in uncomplicated Plasmodium falciparum malaria
(1994) In American Journal of Tropical Medicine and Hygiene 51(3). p.9-372- Abstract
To explain the observation that acute Plasmodium falciparum malaria is associated with a transient inability of peripheral blood cells to respond to antigenic stimulation in vitro, we have postulated the disease-induced reallocation of peripheral lymphocytes, possibly by adhesion to inflamed endothelium. We measured plasma levels of soluble markers of endothelial inflammation and T cell activation in 32 patients suffering from acute, uncomplication P. falciparum malaria, as well as in 10 healthy, aparasitemic control donors. All donors were residents of a malaria-endemic area of Eastern State Sudan. In addition, we measured the T cell surface expression of the interleukin-2 receptor (CD25) and the lymphocyte function-associated antigen... (More)
To explain the observation that acute Plasmodium falciparum malaria is associated with a transient inability of peripheral blood cells to respond to antigenic stimulation in vitro, we have postulated the disease-induced reallocation of peripheral lymphocytes, possibly by adhesion to inflamed endothelium. We measured plasma levels of soluble markers of endothelial inflammation and T cell activation in 32 patients suffering from acute, uncomplication P. falciparum malaria, as well as in 10 healthy, aparasitemic control donors. All donors were residents of a malaria-endemic area of Eastern State Sudan. In addition, we measured the T cell surface expression of the interleukin-2 receptor (CD25) and the lymphocyte function-associated antigen (LFA-1; CD11a/CD18). We found that the plasma levels of all inflammation and activation markers were significantly increased in the malaria patients compared with the control donors. In addition, we found a disease-induced depletion of T cells with high expression of the LFA-1 antigen, particularly in the CD4+ subset. The results obtained provide further support for the hypothesis of T cell reallocation to inflamed endothelium in acute P. falciparum malaria.
(Less)
- author
- Elhassan, I M ; Hviid, L ; Satti, G ; Akerstrom, B LU ; Jakobsen, P H ; Jensen, J B and Theander, T G
- organization
- publishing date
- 1994-09
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- Adolescent, Adult, Animals, Cell Adhesion, Cell Adhesion Molecules/blood, Confidence Intervals, Cross-Sectional Studies, E-Selectin, Endothelium, Vascular/pathology, Female, Humans, Immunophenotyping, Inflammation, Intercellular Adhesion Molecule-1/blood, Lymphocyte Activation, Lymphocyte Function-Associated Antigen-1/blood, Malaria, Falciparum/immunology, Male, Middle Aged, T-Lymphocytes/immunology, Vascular Cell Adhesion Molecule-1
- in
- American Journal of Tropical Medicine and Hygiene
- volume
- 51
- issue
- 3
- pages
- 9 - 372
- publisher
- American Society of Tropcial Medicine & Hygiene
- external identifiers
-
- pmid:7524374
- scopus:0028003622
- ISSN
- 1476-1645
- DOI
- 10.4269/ajtmh.1994.51.372
- language
- English
- LU publication?
- yes
- id
- fef6ec91-21ac-4077-aff2-76b494864ebe
- date added to LUP
- 2019-05-22 10:21:59
- date last changed
- 2024-04-02 04:32:17
@article{fef6ec91-21ac-4077-aff2-76b494864ebe,
abstract = {{<p>To explain the observation that acute Plasmodium falciparum malaria is associated with a transient inability of peripheral blood cells to respond to antigenic stimulation in vitro, we have postulated the disease-induced reallocation of peripheral lymphocytes, possibly by adhesion to inflamed endothelium. We measured plasma levels of soluble markers of endothelial inflammation and T cell activation in 32 patients suffering from acute, uncomplication P. falciparum malaria, as well as in 10 healthy, aparasitemic control donors. All donors were residents of a malaria-endemic area of Eastern State Sudan. In addition, we measured the T cell surface expression of the interleukin-2 receptor (CD25) and the lymphocyte function-associated antigen (LFA-1; CD11a/CD18). We found that the plasma levels of all inflammation and activation markers were significantly increased in the malaria patients compared with the control donors. In addition, we found a disease-induced depletion of T cells with high expression of the LFA-1 antigen, particularly in the CD4+ subset. The results obtained provide further support for the hypothesis of T cell reallocation to inflamed endothelium in acute P. falciparum malaria.</p>}},
author = {{Elhassan, I M and Hviid, L and Satti, G and Akerstrom, B and Jakobsen, P H and Jensen, J B and Theander, T G}},
issn = {{1476-1645}},
keywords = {{Adolescent; Adult; Animals; Cell Adhesion; Cell Adhesion Molecules/blood; Confidence Intervals; Cross-Sectional Studies; E-Selectin; Endothelium, Vascular/pathology; Female; Humans; Immunophenotyping; Inflammation; Intercellular Adhesion Molecule-1/blood; Lymphocyte Activation; Lymphocyte Function-Associated Antigen-1/blood; Malaria, Falciparum/immunology; Male; Middle Aged; T-Lymphocytes/immunology; Vascular Cell Adhesion Molecule-1}},
language = {{eng}},
number = {{3}},
pages = {{9--372}},
publisher = {{American Society of Tropcial Medicine & Hygiene}},
series = {{American Journal of Tropical Medicine and Hygiene}},
title = {{Evidence of endothelial inflammation, T cell activation, and T cell reallocation in uncomplicated Plasmodium falciparum malaria}},
url = {{http://dx.doi.org/10.4269/ajtmh.1994.51.372}},
doi = {{10.4269/ajtmh.1994.51.372}},
volume = {{51}},
year = {{1994}},
}