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Infection and Immunity, December 2002, p. 6628-6637, Vol. 70, No. 12
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.12.6628-6637.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Anomalous Role of Tumor Necrosis Factor Alpha in Experimental Enterococcal Infection

Christopher J. Papasian,1* Richard Silverstein,2 Jian Jun Gao,1 David M. Bamberger,3 and David C. Morrison1,4,5

Departments of Basic Medical Science,1 Internal Medicine,3 Surgery, School of Medicine, University of Missouri—Kansas City, Kansas City, Missouri 64108,4 Department of Biochemistry and Molecular Biology, University of Kansas Medical Center, Kansas City, Kansas 66160,2 Office of Medical Research Administration, Saint Luke's Hospital, Kansas City, Missouri 641115

Received 8 May 2002/ Returned for modification 5 September 2002/ Accepted 20 September 2002

The murine D-galactosamine (D-gal) model of tumor necrosis factor alpha (TNF-{alpha}) hypersensitization was used as an initial tool to investigate the potential contribution of TNF-{alpha} to lethal intraperitoneal (i.p.) infection with Enterococcus faecalis. D-gal sensitized mice to lethal E. faecalis infection, whereas dexamethasone and neutralizing anti-TNF-{alpha} antibody protected D-gal-treated, E. faecalis-infected mice, implicating TNF-{alpha} in the lethal response to E. faecalis infection in D-gal-treated mice. Circulating TNF-{alpha} was undetectable for at least 8 h following i.p. E. faecalis infection, although low peritoneal levels of TNF-{alpha} were detected within 3 h, suggesting that localized TNF-{alpha} production contributed to the lethal response to E. faecalis infection in D-gal-treated mice. Although i.p. E. faecalis infection failed to induce a detectable systemic TNF-{alpha} response, circulating Interleukin-6 (IL-6) was detected within 3 h of infection. IL-6 was also detected in the peritoneum within an hour of infection, prior to the appearance of peritoneal TNF-{alpha}. In striking contrast to in vivo results, E. faecalis induced a potent and rapid TNF-{alpha} response from both mouse peritoneal macrophages and the RAW 264.7 cell line in vitro. This led us to hypothesize that TNF-{alpha} production in response to E. faecalis infection is suppressed by IL-6 in vivo. In vitro experiments demonstrated a statistically significant, but modest, inhibitory effect of IL-6 on TNF-{alpha} production by RAW cells stimulated with E. faecalis. Collectively, these data indicate that acute, lethal E. faecalis infection appears to induce an unusual cytokine response that differs in character from that previously described for most other gram-positive and gram-negative bacteria.

* Corresponding author. Mailing address: Department of Basic Medical Science-M3-C03, UMKC School of Medicine, 2411 Holmes St., Kansas City, MO 64108. Phone: (816) 235-2299. Fax: (816) 235-6517. E-mail: papasianc{at}umkc.edu.

Editor: J. T. Barbieri

Infection and Immunity, December 2002, p. 6628-6637, Vol. 70, No. 12
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.12.6628-6637.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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