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Am. J. Trop. Med. Hyg., 80(5), 2009, pp. 718-722
Copyright © 2009 by The American Society of Tropical Medicine and Hygiene

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SHORT REPORT


Disruption of Nod-like Receptors Alters Inflammatory Response to Infection but Does Not Confer Protection in Experimental Cerebral Malaria

Constance A. M. Finney{dagger}, Ziyue Lu{dagger}, Lionel LeBourhis, Dana J. Philpott, AND Kevin C. Kain*
Tropical Disease Unit, Division of Infectious Diseases, Department of Medicine, Toronto General Hospital, University Health Network, Toronto, Ontario, Canada; McLaughlin-Rotman Centre for Global Health, McLaughlin Centre for Molecular Medicine, University of Toronto, Toronto, Ontario, Canada; Department of Immunology, University of Toronto, Toronto, Ontario, Canada

 

ABSTRACT

Research relating to host inflammatory processes during malaria infection has focused on Toll-like receptors, membrane-bound receptors implicated in innate sensing, and phagocytosis of parasitized erythrocytes by host cells. This is the first study to examine the role of Nod proteins, members of the Nod-like receptor (NLR) family of cytoplasmic proteins involved in pathogen recognition, in a murine model of cerebral malaria (Plasmodium berghei ANKA, PbA). Here, we find that nod1nod2–/– mice infected with PbA show no difference in survival or parasitemia compared with wild-type infected animals. However, cytokine levels, notably those associated with NLR activation including interleukin (IL)1-β, KC, and MCP-1, and proteins linked to malaria pathogenesis, such as interferon-{gamma} (IFN-{gamma}), were decreased in the nod-1nod2–/– animals. We therefore demonstrate for the first time that Nod proteins are activated in response to parasites, and they play a role in regulating host inflammatory responses during malaria infection.

Received May 12, 2008. Accepted for publication January 18, 2009.

Financial support: This study was funded in part by a Canadian Institutes of Health Research (CIHR) Team Grant in Malaria (KCK), CIHR MT-13721 (KCK), Genome Canada through the Ontario Genomics Institute (KCK), CIHR Canada Research Chair (KCK).

Disclaimer: The funding agency had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

* Address correspondence to Kevin C. Kain, Toronto General Hospital, University Health Network, 200 Elizabeth Street, EN 13-214, Toronto, Ontario, Canada M5G 2C4. E-mail: Kevin.Kain{at}uhn.on.ca

{dagger} C. Finney and Z. Lu contributed equally to this work.

Authors’ addresses: Constance Finney and Ziyue Lu, McLaughlin-Rotman Centre, MaRS, TMDT, 101 College Street, Suite 10-401, Toronto, ON, Canada M5G 1L7. Lionel LeBourhis and Dana Philpott, Department of Immunology, Medical Sciences Building, University of Toronto, Toronto, ON, Canada M5S 1A8. Kevin C. Kain, Toronto General Hospital, University Health Network, 200 Elizabeth Street, EN 13-214, Toronto, Ontario, Canada M5G 2C4, Tel: 416-340-3535, Fax: 416-595-5826, E-mail: Kevin.Kain{at}uhn.on.ca.




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Copyright © 2009 by the American Society of Tropical Medicine and Hygiene.