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Research ArticleArticle

Treatment with Liposome-Bound Recombinant Human Tumor Necrosis Factor-α Suppresses Parasitemia and Protects againstPlasmodium berghei k173-Induced Experimental Cerebral Malaria in Mice

N. S. Postma, D. J. A. Crommelin, W. M. C. Eling and J. Zuidema
Journal of Pharmacology and Experimental Therapeutics January 1999, 288 (1) 114-120;
N. S. Postma
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D. J. A. Crommelin
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W. M. C. Eling
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J. Zuidema
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Abstract

Our study describes liposomes (conventional or sterically stabilized) as carrier systems for recombinant human tumor necrosis factor-α (rhTNF-α) to increase its protective efficacy againstPlasmodium berghei-induced experimental cerebral malaria (ECM) in mice. rhTNF-α was either covalently coupled to the outer surface of preformed liposomes or encapsulated into the liposomes. For coupling to the liposomes, reactive thiol groups were introduced in rhTNF-α by reaction with N-succinimidylS-acetylthioacetate. Intravenous injection of liposome-bound rhTNF-α substantially enhanced protection against ECM as compared with injection of free rhTNF-α. A similar protective efficacy against ECM was obtained by treatment with rhTNF-α coupled to either conventional or sterically stabilized liposomes. Encapsulation of rhTNF-α into liposomes did not improve the protective efficacy of rhTNF-α against P. berghei-induced ECM. Parasitemia was suppressed by treatment with either free or liposome-bound rhTNF-α in mice protected against ECM, but not in rhTNF-α-treated mice developing ECM. These data suggest that the effect of rhTNF-α on parasitemia plays a role in establishing protection against ECM. Our studies indicate that liposome-bound rhTNF-α exhibits an enhanced protective efficacy against ECM compared with free rhTNF-α. It is hypothesized that thiolation of rhTNF-α and coupling to the liposomal bilayer stabilizes the bioactive trimeric configuration of rhTNF-α.

Footnotes

  • Send reprint requests to: D.J.A. Crommelin, Department of Pharmaceutics, Utrecht University, PO Box 80082, 3508 TB Utrecht, The Netherlands. E-mail:D.J.A.Crommelin{at}pharm.uu.nl

  • ↵1 Current address: Department of Medical Microbiology, University Hospital Nijmegen, PO Box 9101, 6500 HB Nijmegen, The Netherlands.

  • Abbreviations:
    Chol
    cholesterol
    PEG
    polyethylene glycol
    ECM
    experimental cerebral malaria
    EPC
    egg phosphatidylcholine
    HSA
    human serum albumin
    MPB-PE
    maleimido-4-(p-phenylbutyrate)-phosphatidylethanolamine
    PEG-DSPE
    distearoylphosphatidylethanolamine-polyethylene glycol 2000
    SATA
    N-succinimidyl S-acetylthioacetate
    rhTNF-α
    recombinant human tumor necrosis factor-α
    rhTNFα-ATA
    acetylthioacetyl-rhTNF-α
    • Received April 28, 1998.
    • Accepted July 30, 1998.
  • The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics: 288 (1)
Journal of Pharmacology and Experimental Therapeutics
Vol. 288, Issue 1
1 Jan 1999
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Research ArticleArticle

Treatment with Liposome-Bound Recombinant Human Tumor Necrosis Factor-α Suppresses Parasitemia and Protects againstPlasmodium berghei k173-Induced Experimental Cerebral Malaria in Mice

N. S. Postma, D. J. A. Crommelin, W. M. C. Eling and J. Zuidema
Journal of Pharmacology and Experimental Therapeutics January 1, 1999, 288 (1) 114-120;

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Research ArticleArticle

Treatment with Liposome-Bound Recombinant Human Tumor Necrosis Factor-α Suppresses Parasitemia and Protects againstPlasmodium berghei k173-Induced Experimental Cerebral Malaria in Mice

N. S. Postma, D. J. A. Crommelin, W. M. C. Eling and J. Zuidema
Journal of Pharmacology and Experimental Therapeutics January 1, 1999, 288 (1) 114-120;
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