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      The Case for the Use of PPAR γ Agonists as an Adjunctive Therapy for Cerebral Malaria

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      Journal: PPAR Research
      Publisher: Hindawi Publishing Corporation

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          Abstract

          Cerebral malaria is a severe complication of Plasmodium falciparum infection associated with high mortality even when highly effective antiparasitic therapy is used. Adjunctive therapies that modify the pathophysiological processes caused by malaria are a possible way to improve outcome. This review focuses on the utility of PPAR γ agonists as an adjunctive therapy for the treatment of cerebral malaria. The current knowledge of PPAR γ agonist use in malaria is summarized. Findings from experimental CNS injury and disease models that demonstrate the potential for PPAR γ agonists as an adjunctive therapy for cerebral malaria are also discussed.

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          The global distribution of clinical episodes of Plasmodium falciparum malaria.

          Robert W. Snow, Carlos Guerra, Abdisalan Noor … (2005)
          Interest in mapping the global distribution of malaria is motivated by a need to define populations at risk for appropriate resource allocation and to provide a robust framework for evaluating its global economic impact. Comparison of older and more recent malaria maps shows how the disease has been geographically restricted, but it remains entrenched in poor areas of the world with climates suitable for transmission. Here we provide an empirical approach to estimating the number of clinical events caused by Plasmodium falciparum worldwide, by using a combination of epidemiological, geographical and demographic data. We estimate that there were 515 (range 300-660) million episodes of clinical P. falciparum malaria in 2002. These global estimates are up to 50% higher than those reported by the World Health Organization (WHO) and 200% higher for areas outside Africa, reflecting the WHO's reliance upon passive national reporting for these countries. Without an informed understanding of the cartography of malaria risk, the global extent of clinical disease caused by P. falciparum will continue to be underestimated.
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            PPAR-gamma agonists inhibit production of monocyte inflammatory cytokines.

            C. Jiang, A. Ting, B. Seed (1998)
            The peroxisome proliferator-activated receptor-gamma (PPAR-gamma) is a member of the nuclear receptor family of transcription factors, a large and diverse group of proteins that mediate ligand-dependent transcriptional activation and repression. Expression of PPAR-gamma is an early and pivotal event in the differentiation of adipocytes. Several agents that promote differentiation of fibroblast lines into adipocytes have been shown to be PPAR-gamma agonists, including several prostanoids, of which 15-deoxy-delta-prostaglandin J2 is the most potent, as well as members of a new class of oral antidiabetic agents, the thiazolidinediones, and a variety of non-steroidal anti-inflammatory drugs (NSAIDs). Here we show that PPAR-gamma agonists suppress monocyte elaboration of inflammatory cytokines at agonist concentrations similar to those found to be effective for the promotion of adipogenesis. Inhibition of cytokine production may help to explain the incremental therapeutic benefit of NSAIDs observed in the treatment of rheumatoid arthritis at plasma drug concentrations substantially higher than are required to inhibit prostaglandin G/H synthase (cyclooxygenase).
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              Carbon monoxide has anti-inflammatory effects involving the mitogen-activated protein kinase pathway.

              L Otterbein, F H Bach, J. Alam … (2000)
              The stress-inducible protein heme oxygenase-1 provides protection against oxidative stress. The anti-inflammatory properties of heme oxygenase-1 may serve as a basis for this cytoprotection. We demonstrate here that carbon monoxide, a by-product of heme catabolism by heme oxygenase, mediates potent anti-inflammatory effects. Both in vivo and in vitro, carbon monoxide at low concentrations differentially and selectively inhibited the expression of lipopolysaccharide-induced pro-inflammatory cytokines tumor necrosis factor-alpha, interleukin-1beta, and macrophage inflammatory protein-1beta and increased the lipopolysaccharide-induced expression of the anti-inflammatory cytokine interleukin-10. Carbon monoxide mediated these anti-inflammatory effects not through a guanylyl cyclase-cGMP or nitric oxide pathway, but instead through a pathway involving the mitogen-activated protein kinases. These data indicate the possibility that carbon monoxide may have an important protective function in inflammatory disease states and thus has potential therapeutic uses.
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                Author and article information

                Journal
                Journal ID (nlm-ta): PPAR Res
                Journal ID (publisher-id): PPAR
                Title: PPAR Research
                Publisher: Hindawi Publishing Corporation
                ISSN (Print): 1687-4757
                ISSN (Electronic): 1687-4765
                Publication date (Print): 2012
                Publication date (Electronic): 9 June 2011
                Volume: 2012
                Electronic Location Identifier: 513865
                Affiliations
                Sandra A. Rotman Laboratories, McLaughlin-Rotman Centre for Global Health, Toronto General Hospital, University Health Network, 101 College Street, Suite 10-359, Toronto, ON, Canada M5G 1L7
                Author notes

                Academic Editor: Marion M. Chan

                Article
                DOI: 10.1155/2012/513865
                PMC ID: 3135089
                PubMed ID: 21772838
                SO-VID: 6500ef49-4b99-458b-b976-0c5f8410b1b5
                Copyright © Copyright © 2012 Lena Serghides.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 7 January 2011
                Date accepted : 28 February 2011
                Categories
                Subject: Review Article

                ScienceOpen disciplines: Biochemistry
                Data availability:
                ScienceOpen disciplines: Biochemistry

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