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Suppression of prostaglandin E2 by malaria parasite products and antipyretics promotes overproduction of tumor necrosis factor-alpha: association with the pathogenesis of childhood malarial anemia.

Publication ,  Journal Article
Keller, CC; Davenport, GC; Dickman, KR; Hittner, JB; Kaplan, SS; Weinberg, JB; Kremsner, PG; Perkins, DJ
Published in: J Infect Dis
May 15, 2006

Cytokines and effector molecules are important immunoregulatory molecules in human malaria. Tumor necrosis factor (TNF)-alpha limits malaria parasitemia but also promotes pathogenesis at high concentrations, whereas prostaglandin E2 (PGE2) inhibits TNF-alpha production and is reduced in childhood malaria, at least in part, through suppression of cyclooxygenase (COX)-2 following the ingestion of Plasmodium falciparum hemozoin (pfHz; malarial pigment) by peripheral blood mononuclear cells (PBMCs). Although molecular interactions between TNF-alpha and PGE2 are largely unexplored in human malaria, results presented here show that pfHz-induced suppression of PBMC COX-2 gene products induces overproduction of TNF-alpha. Moreover, addition of exogenous PGE2 to pfHz-treated PBMCs dose-dependently decreased TNF-alpha production, whereas experimental COX inhibitors and antipyretics used during human malaria generated increased TNF-alpha production. Healthy, malaria-exposed children had elevated levels of circulating bicyclo-PGE2/TNF-alpha, compared with children with malarial anemia (P<.01), with systemic bicyclo-PGE2 and TNF-alpha significantly associated with hemoglobin concentrations (r=0.745; P<.01). The results of the present study illustrate that pfHz-induced suppression of PGE2 promotes overproduction of TNF-alpha, which is associated with enhanced malarial anemia.

Duke Scholars

Published In

J Infect Dis

DOI

ISSN

0022-1899

Publication Date

May 15, 2006

Volume

193

Issue

10

Start / End Page

1384 / 1393

Location

United States

Related Subject Headings

  • Tumor Necrosis Factor-alpha
  • Reverse Transcriptase Polymerase Chain Reaction
  • RNA, Messenger
  • Prospective Studies
  • Plasmodium falciparum
  • Phagocytosis
  • Microbiology
  • Male
  • Malaria, Falciparum
  • Longitudinal Studies
 

Citation

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ICMJE
MLA
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Keller, C. C., Davenport, G. C., Dickman, K. R., Hittner, J. B., Kaplan, S. S., Weinberg, J. B., … Perkins, D. J. (2006). Suppression of prostaglandin E2 by malaria parasite products and antipyretics promotes overproduction of tumor necrosis factor-alpha: association with the pathogenesis of childhood malarial anemia. J Infect Dis, 193(10), 1384–1393. https://doi.org/10.1086/503047
Keller, Christopher C., Gregory C. Davenport, Katherine R. Dickman, James B. Hittner, Sandra S. Kaplan, J Brice Weinberg, Peter G. Kremsner, and Douglas J. Perkins. “Suppression of prostaglandin E2 by malaria parasite products and antipyretics promotes overproduction of tumor necrosis factor-alpha: association with the pathogenesis of childhood malarial anemia.J Infect Dis 193, no. 10 (May 15, 2006): 1384–93. https://doi.org/10.1086/503047.
Keller CC, Davenport GC, Dickman KR, Hittner JB, Kaplan SS, Weinberg JB, Kremsner PG, Perkins DJ. Suppression of prostaglandin E2 by malaria parasite products and antipyretics promotes overproduction of tumor necrosis factor-alpha: association with the pathogenesis of childhood malarial anemia. J Infect Dis. 2006 May 15;193(10):1384–1393.
Journal cover image

Published In

J Infect Dis

DOI

ISSN

0022-1899

Publication Date

May 15, 2006

Volume

193

Issue

10

Start / End Page

1384 / 1393

Location

United States

Related Subject Headings

  • Tumor Necrosis Factor-alpha
  • Reverse Transcriptase Polymerase Chain Reaction
  • RNA, Messenger
  • Prospective Studies
  • Plasmodium falciparum
  • Phagocytosis
  • Microbiology
  • Male
  • Malaria, Falciparum
  • Longitudinal Studies