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Am. J. Trop. Med. Hyg., 70(6), 2004, pp. 645-650
Copyright © 2004 by The American Society of Tropical Medicine and Hygiene

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SHORT REPORT: LETHAL MALARIA IN CYTOSOLIC PHOSPHOLIPASE A2- AND PHOSPHOLIPASE A2IIA-DEFICIENT MICE

SHUMPEI ISHIKAWA, NAONORI UOZUMI, TAKASHI SHIIBASHI, TAKASHI IZUMI, MASASHI FUKAYAMA, TAKAO SHIMIZU, JUNICHI WATANABE, AND SADAO NOGAMI
Department of Pathology, and Department of Biochemistry and Molecular Biology, The University of Tokyo, Hongo, Tokyo, Japan; Department of Parasitology, Institute of Medical Science, The University of Tokyo, Shirokanedai, Minatoku, Tokyo, Japan; Department of Veterinary Medicine, Nihon University, Kameino, Fujisawa, Kanagawa, Japan; Department of Biochemistry, Gunma University, School of Medicine, Showamachi, Gunma, Japan

 

ABSTRACT

Lipid mediators play important roles in the pathogenesis of malaria. Phospholipase A2s are enzymes involved in the production of these mediators, and they function in inflammation. Among them, cytosolic phospholipase A2 (cPLA2) is a key enzyme in the metabolism of arachidonic acid, the first intermediate in the production of lipid mediators. Plasmodium berghei ANKA causes cerebral malaria in CL57B/6 mice, and we recently produced cPLA2-deficient mice with this background. With the expectation of reduced pathogenicity, we performed experimental infection in these mice. Unexpectedly, the infected mice developed cerebral malaria and died at the same time as the control mice, while the parasitemia progressed similarly in both groups. These observations suggest that secretory PLA2s rather than cPLA2 may be involved in the aggravation, although possible compensation by the induction of other enzymes has not been excluded. The present findings are expected to help clarify the involvement of various phospholipase A2s in malaria.

Received March 19, 2003. Accepted for publication February 2, 2004.

Acknowledgments: We thank Satoko Oguma ( Nihon University) and the staff of the Department of Pathology of The University of Tokyo for helpful assistance. We are grateful to Dr. E. Nakajima for critical reading of the manuscript.

Financial support: The work was partly supported by a Grant-in-Aid for Promotion of Science from The Ministry of Education and Science (14560273).

Authors’ addresses: Shumpei Ishikawa and Masashi Fukayama, Department of Pathology, The University of Tokyo, 7-3-1 Hongo, Bunkyoku, Tokyo 113-0033, Japan. Naonori Uozumi and Takao Shimizu, Department of Biochemistry and Molecular Biology, The University of Tokyo, 7-3-1 Hongo, Bunkyoku, Tokyo 113-0033, Takashi Shiibashi and Sadao Nogami, Department of Veterinary Medicine, Nihon University, 1866 Kameino, Fujisawa, Kanagawa 252-8510, Japan. Takashi Izumi, Department of Biochemistry, Gunma University, 3-39-22 Showamachi, Maebashi, Gunma 371-8511, Japan. Junichi Watanabe, Department of Parasitology, Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minatoku, Tokyo 108-8639, Japan, Telephone: 81-3-5449-5378, Fax: 81-3-5689-3979, E-mail: jwatanab{at}ims.u-tokyo.ac.jp.






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Copyright © 2004 by the American Society of Tropical Medicine and Hygiene.