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Infection and Immunity, May 1999, p. 2306-2311, Vol. 67, No. 5
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Transforming Growth Factor beta -Induced Failure of Resistance to Infection with Blood-Stage Plasmodium chabaudi in Mice

Naohisa Tsutsui,1,2 and Tsuneo Kamiyama1,*

Department of Veterinary Science, National Institute of Infectious Diseases, Shinjuku-ku, Tokyo 162-8640,1 and Yokohama Research Center, Mitsubishi Chemical Co., Aoba-ku, Yokohama 227-8502,2 Japan

Received 6 November 1998/Returned for modification 16 December 1998/Accepted 22 February 1999

The role of transforming growth factor beta  (TGF-beta ) in infection with Plasmodium chabaudi was investigated with resistant and susceptible mouse models. C57BL/10 mice produced gamma interferon (IFN-gamma ) and nitric oxide (NO) shortly after infection and cleared the parasite spontaneously. In contrast, BALB/c mice showed a transient enhancement of TGF-beta production, followed by a relative lack of IFN-gamma and NO production, and succumbed to the infection. However, there was no correlation between levels of serum TGF-beta and splenic TGF-beta mRNA in both mouse strains before and after infection. Administration of recombinant TGF-beta (rTGF-beta ) rendered resistant mice susceptible because of suppression of subsequent production of IFN-gamma and NO. Administration of anti-TGF-beta antibody to the infected BALB/c mice resulted in remarkable increases in serum IFN-gamma and NO, and the mice resisted the infection. Splenic CD4+ T and CD11b+ cells of C57BL/10 mice were significantly activated after infection, but this was completely abrogated by administration of rTGF-beta . These results suggested that, in the P. chabaudi-susceptible but not resistant mice, production of TGF-beta was promoted, and subsequent failure of IFN-gamma - and NO-dependent resistance to the parasite was induced. This study is the first to indicate that TGF-beta production was the key event in failure of resistance to mouse malaria.

* Corresponding author. Mailing address: Department of Veterinary Science, National Institute of Infectious Diseases, Toyama 1-23-1, Shinjuku-ku, Tokyo 162-8640, Japan. Phone: 81-3-5285-1111, ext. 2622. Fax: 81-5285-1179. E-mail: kamiyama{at}nih.go.jp.

Infection and Immunity, May 1999, p. 2306-2311, Vol. 67, No. 5
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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