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Am. J. Trop. Med. Hyg., 75(1), 2006, pp. 178-181
Copyright © 2006 by The American Society of Tropical Medicine and Hygiene

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SHORT REPORT


ROLE OF TYPE I/II SCAVENGER RECEPTORS IN MALARIAL INFECTION IN C57BL/6J MICE

MAI INOUE, XUENAN XUAN, KOZO FUJISAKI, IKUO IGARASHI, AND HIROSHI SUZUKI*
Research Unit for Functional Genomics, National Research Center for Protozoan Diseases, Obihiro University of Agriculture and Veterinary Medicine, Obihiro, Hokkaido, Japan; Department of Developmental and Medical Technology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan

 

ABSTRACT

Although it is well known that SR-A I/II plays a significant role in host defense against bacterial and viral infection, the contribution of SR-A I/II to protozoan infection is not well understood. Thus, we examined the possible role of SR-A I/II against murine malarial infection, such as Plasmodium. berghei and P. yoelli, by using SR-A I/II knockout mice with a C57BL/6J genetic background. When SR-A I/II knockout mice were infected with P. berghei NK65 or P. yoelli 17X, their survival rates were not significantly different from wild-type animals. In terms of the kinetics of parasitemia, hematocrit values and the number of white blood cells, there were no significant differences between the genotypes in P. berghei NK65 or P. yoelli 17X infection. Taken together with the findings in our previous report, the SR-A I/II functional contribution to host defense in malarial infection does not seem to be widely extended, and the effect of SR-A I/II seem in collaboration with other, as yet unidentified, gene(s).

Received August 31, 2005. Accepted for publication February 12, 2006.

Acknowledgments: The authors thank Y. Ueta, C. Ichikawa, M. Chiba, M. Kim, T. Ishijima, K. Maeda, T. Hori, D. Lee, J. Lee, and T. Asano for technical assistance for breeding animals. We are also grateful to Drs. Waki (Gunma Prefectural College of Health Science) and Suzuki (Gunma University, School of Medicine) for P. berghei NK65 and Dr. Kobayashi (Kyorin University, School of Medicine) for P. yoelii 17X. Pacific Edit reviewed the manuscript before submission.

Financial support: This study was supported, in part, by a grant from Special Coordination Fund for Promoting Science and Technology, Ministry of Education, Culture, Sports, Science, Japan.

* Address correspondence to Hiroshi Suzuki, Research Unit for Functional Genomics, National Research Center for Protozoan Diseases, Obihiro University of Agriculture and Veterinary Medicine, Nishi 2-13, Inada, Obihiro, Hokkaido 080-8555, Japan. E-mail: hisuzuki{at}obihiro.ac.jp

Authors’ addresses: Mai Inoue, Xuenan Xuan, Kozo Fujisaki, Ikuo Igarashi, and Hiroshi Suzuki, Research Unit for Functional Genomics, National Research Center for Protozoan Diseases, Obihiro University of Agriculture and Veterinary Medicine, Nishi 2–13, Inada, Obihiro, Hokkaido 080-8555, Japan. Hiroshi Suzuki, Department of Developmental and Medical Technology, Graduate School of Medicine, The University of Tokyo, 7-3-1, Hongo, Bunkyo-ku, Tokyo 113-0033, Japan, E-mail: hisuzuki{at}obihiro.ac.jp.






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Copyright © 2006 by the American Society of Tropical Medicine and Hygiene.