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Infection and Immunity, May 1999, p. 2660-2664, Vol. 67, No. 5
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Deficiency in Tumor Necrosis Factor Alpha Activity Does Not Impair Early Protective Th1 Responses against Blood-Stage Malaria

Hakeem Sam, Zhong Su, and Mary M. Stevenson*

McGill University Centre for the Study of Host Resistance and Montreal General Hospital Research Institute, Montreal, Quebec, Canada

Received 11 November 1998/Returned for modification 5 January 1999/Accepted 22 February 1999

Blood-stage Plasmodium chabaudi AS infection was controlled by 4 weeks in mice with deletion of tumor necrosis factor p55 and p75 receptors (TNFR-knockout [KO]) and control wild-type (WT) mice, although female TNFR-KO mice showed slightly but significantly higher parasitemia immediately following the peak. Serum interleukin 12 (IL-12) p70 and gamma interferon (IFN-gamma ) levels were similar but tumor necrosis factor alpha levels were significantly higher in TNFR-KO mice than in WT controls. Splenic IL-12 receptor beta 1 and beta 2 and IFN-gamma mRNA expression, as well as spleen cell production of IFN-gamma and IL-4, were comparable in both mouse types, but IL-10 production was significantly higher in cells from TNFR-KO mice than in cells from WT mice. Lipopolysaccharide-induced NO secretion by splenic macrophages in vitro was significantly reduced but systemic NO3- levels were similar in infected TNFR-KO and WT mice.

* Corresponding author. Mailing address: Montreal General Hospital Research Institute, 1650 Cedar Ave., Montreal, Quebec H3G 1A4, Canada. Phone: (514) 937-6011, ext. 4507. Fax: (514) 934-8332. E-mail: mcev{at}musica.mcgill.ca.

Infection and Immunity, May 1999, p. 2660-2664, Vol. 67, No. 5
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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