AJTMH Transactions of the Royal Society of Tropical Medicine and Hygiene
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am. J. Trop. Med. Hyg., 41(2), 1989, pp. 144-160
Copyright © 1989 by The American Society of Tropical Medicine and Hygiene

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Weiss, L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Weiss, L.

Mechanisms of Splenic Control of Murine Malaria: Cellular Reactions of the Spleen in Lethal (Strain 17XL) Plasmodium Yoelii Malaria in BALB/c Mice, and the Consequences of Pre-Infective Splenectomy

Leon Weiss
School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania

The splenic response in lethal 17XL Plasmodium yoelii murine malaria is vigorous, displaying marked phagocytosis, erythropoiesis, lymphopoiesis, plasmacytopoiesis, and, from day 3 of infection, increasing levels of parasitized erythrocytes. There is also a pronounced response of newly characterized fibroblastic stromal cells which branch and fuse with one another, forming extensive, complex, irregular, syncytial membranous sheets which provide a variety of barriers. Hence, I term these barrier cells (BC), and their fusion results in barrier-forming complexes (BFC). BC form adherent surfaces, trapping parasitized erythrocytes and monocytes-macrophages, facilitating phagocytosis. They envelop single plasma cells, erythrocytes, erythroblasts, lymphocytes, reticulocytes, monocytes-macrophages, or clusters of them. They surround blood vessels, forming blood-spleen barriers. They are insinuated into the circumferential reticulum at the periphery of white pulp, isolating white pulp. They form channels in red pulp, directing blood flow. They are associated with collagen. There appear to be several sources of BC. They may originate by activation of established reticular cells which form the filtration beds, by activation of reticular cells covering the pulp surface of capsule and trabeculae, and as a major source in this malaria, from circulating progenitors entering the splenic pulp from the vasculature. In non-lethal malaria, these barrier systems protect splenic reticulocytes from parasitization. In the lethal 17XL malaria they do not, and there follows a considerable increase in parasitization in the spleen with a corresponding increase in active macrophages. Largescale parasitization and parasite recycling through the great stores of splenic reticulocytes in the lethal malaria, and the failure of parasitization of these splenic reticulocytes reserves on the non-lethal malaria, suggests that the actions of the spleen aggravate the lethal malaria and ameliorate the non-lethal. This is supported by the finding that non-lethal malaria is aggravated and lethal malaria ameliorated by splenectomy.




This article has been cited by other articles:


Home page
 BloodHome page
I. Safeukui, J.-M. Correas, V. Brousse, D. Hirt, G. Deplaine, S. Mule, M. Lesurtel, N. Goasguen, A. Sauvanet, A. Couvelard, et al.
Retention of Plasmodium falciparum ring-infected erythrocytes in the slow, open microcirculation of the human spleen
Blood, September 15, 2008; 112(6): 2520 - 2528.
[Abstract] [Full Text] [PDF]

Home page
 Infect. Immun.Home page
E. T. Cadman, A. Y. Abdallah, C. Voisine, A.-M. Sponaas, P. Corran, T. Lamb, D. Brown, F. Ndungu, and J. Langhorne
Alterations of Splenic Architecture in Malaria Are Induced Independently of Toll-Like Receptors 2, 4, and 9 or MyD88 and May Affect Antibody Affinity
Infect. Immun., September 1, 2008; 76(9): 3924 - 3931.
[Abstract] [Full Text] [PDF]

Home page
 J. Immunol.Home page
Y. Miyazaki, M. Bunting, D. M. Stafforini, E. S. Harris, T. M. McIntyre, S. M. Prescott, V. S. Frutuoso, F. C. Amendoeira, D. de Oliveira Nascimento, A. Vieira-de-Abreu, et al.
Integrin {alpha}D 2 Is Dynamically Expressed by Inflamed Macrophages and Alters the Natural History of Lethal Systemic Infections
J. Immunol., January 1, 2008; 180(1): 590 - 600.
[Abstract] [Full Text] [PDF]

Home page
 Infect. Immun.Home page
K. N. Couper, D. G. Blount, J. C. R. Hafalla, N. van Rooijen, J. B. de Souza, and E. M. Riley
Macrophage-Mediated but Gamma Interferon-Independent Innate Immune Responses Control the Primary Wave of Plasmodium yoelii Parasitemia
Infect. Immun., December 1, 2007; 75(12): 5806 - 5818.
[Abstract] [Full Text] [PDF]

Home page
 BloodHome page
A. A. Lamikanra, D. Brown, A. Potocnik, C. Casals-Pascual, J. Langhorne, and D. J. Roberts
Malarial anemia: of mice and men
Blood, July 1, 2007; 110(1): 18 - 28.
[Abstract] [Full Text] [PDF]

Home page
 J. Immunol.Home page
L. Beattie, C. R. Engwerda, M. Wykes, and M. F. Good
CD8+ T Lymphocyte-Mediated Loss of Marginal Metallophilic Macrophages following Infection with Plasmodium chabaudi chabaudi AS
J. Immunol., August 15, 2006; 177(4): 2518 - 2526.
[Abstract] [Full Text] [PDF]

Home page
 Infect. Immun.Home page
J. Poovassery and J. M. Moore
Murine Malaria Infection Induces Fetal Loss Associated with Accumulation of Plasmodium chabaudi AS-Infected Erythrocytes in the Placenta.
Infect. Immun., May 1, 2006; 74(5): 2839 - 2848.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1989 by the American Society of Tropical Medicine and Hygiene.