Advanced Search

Journal Navigation

Journal Home

Subscriptions

Archive

Contact Us

Table of Contents

Click here to sign up for SAGE Journal Email Alerts today!

Sign In to gain access to subscriptions and/or personal tools.
Journal of Endotoxin Research
This Article
Right arrow Full Text (PDF)
Right arrow References
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Alert me to new issues of the journal
Right arrow Add to Saved Citations
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Request Reprints
Right arrow Add to My Marked Citations
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Right arrow Citing Articles via Scopus
Google Scholar
Right arrow Articles by Silverstein, R.
Right arrow Articles by Morrison, D.C.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Silverstein, R.
Right arrow Articles by Morrison, D.C.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?

Fundamental differences during Gram-positive versus Gram-negative sepsis become apparent during bacterial challenge of D-galactosamine-treated mice

R. Silverstein

Department of Biochemistry and Molecular Biology, University of Kansas Medical Center, Kansas City, Kansas, USA

M. Norimatsu

Department of Microbiology, Molecular Genetics and Immunology, University of Kansas Medical Center, Kansas City, Kansas, USA

D.C. Morrison

Department of Microbiology, Molecular Genetics and Immunology, University of Kansas Medical Center, Kansas City, Kansas, USA

Gram-negative and Gram-positive bacteria have been compared with respect to lethal effects when each is administered to normal and D-galactosamine-sensitized mice, both with and without concomitant dexamethasone treatment. In the case of Escherichia coli, the extent of sensitization by D-galactosamine treatment (10,000-fold) and the relative magnitude of the corresponding protection with dexamethasone (150-fold) are both consistent with an expected significant role of LPS in production of TNF{alpha} that then mediates lethal toxicity. With Staphylococcus aureus, however, marginal sensitization by D-galactosamine (5-fold) and a corresponding lack of dexamethasone protection indicate a reduced role for TNF{alpha} as a lethal mediator. In vitro comparisons of TNF{alpha} release from E. coli and S. aureus stimulated peritoneal macrophages (100-fold difference) add further support to this conclusion. Endotoxin hypo-responsive mice (C3H/HeJ) infected with E. coli are not protected by dexamethasone. Each of these comparisons indicate that the contribution of TNF{alpha} to the pathophysiological manifestations of experimental sepsis may vary substantially even among extracellular bacteria and, correspondingly, that differential dexamethasone protection may serve a discriminatory function for the potential involvement of this cytokine.

Journal of Endotoxin Research, Vol. 4, No. 3, 173-181 (1997)
DOI: 10.1177/096805199700400302


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?


This article has been cited by other articles:


Home page
Innate ImmunityHome page
C. Hermann
Review: Variability of host pathogen interaction
Innate Immunity, August 1, 2007; 13(4): 199 - 218.
[Abstract] [PDF]