help button home button Am J Pathol ASIP MEMBERSHIP
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Order Full text via Infotrieve
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Ulich, T. R.
Right arrow Articles by del Castillo, J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ulich, T. R.
Right arrow Articles by del Castillo, J.

American Journal of Pathology, Vol 134, 11-14, Copyright © 1989 by American Society for Investigative Pathology


REGULAR ARTICLES

Endotoxin-induced cytokine gene expression in vivo. I. Expression of tumor necrosis factor mRNA in visceral organs under physiologic conditions and during endotoxemia

TR Ulich, K Guo and J del Castillo
Department of Pathology, UC Irvine School of Medicine 92717.

Tumor necrosis factor (TNF) mRNA was detected by Northern blotting in whole-organ homogenates of the spleen, liver, kidney, lung, and small bowel in naive and saline-injected control rats, supporting the hypothesis that TNF mRNA is present in vivo in a preformed intracellular pool. TNF mRNA in endotoxin-treated rats as quantitated by densitometry of the ratio of TNF mRNA to actin mRNA in Northern blots was present in increased quantity in the liver, kidney, and lung (1.6-2.9 times over time zero levels) at 15 minutes and increased quantity in the spleen, liver, and kidney (1.3-1.9 times over time zero levels) at 30 minutes. The kinetics of endotoxin-induced TNF gene expression are consistent with the relatively transient peak of serum TNF protein levels reported by previous investigators to occur approximately 1 hour after injection of endotoxin. Because TNF mRNA appeared ubiquitous in the organs of control rats examined and because the endotoxin-induced increase in TNF mRNA was relatively small, endotoxin may induce the expression of the TNF protein in serum not only by increasing TNF mRNA levels but perhaps more importantly by a posttranscriptional mechanism. The presence of a preformed pool of TNF mRNA may teleologically be viewed as a mechanism to increase the rapidity of the host's response to sepsis.


This article has been cited by other articles:


Home page
Infect. Immun.Home page
C. A. Salkowski, G. Detore, A. Franks, M. C. Falk, and S. N. Vogel
Pulmonary and Hepatic Gene Expression following Cecal Ligation and Puncture: Monophosphoryl Lipid A Prophylaxis Attenuates Sepsis-Induced Cytokine and Chemokine Expression and Neutrophil Infiltration
Infect. Immun., August 1, 1998; 66(8): 3569 - 3578.
[Abstract] [Full Text] [PDF]


Home page
J. Exp. Med.Home page
Y. Yang, J.-F. Chang, J. R. Parnes, and C. Garrison Fathman
T Cell Receptor (TCR) Engagement Leads to Activation-induced Splicing of  Tumor Necrosis Factor (TNF) Nuclear Pre-mRNA
J. Exp. Med., July 20, 1998; 188(2): 247 - 254.
[Abstract] [Full Text] [PDF]


Home page
Innate ImmunityHome page
M.T. Demitri, M. Velucchi, L. Bracci, A. Rustici, M. Porro, P. Villa, and P. Ghezzi
Inhibition of LPS-induced systemic and local TNF production by a synthetic anti-endotoxin peptide (SAEP-2)
Innate Immunity, December 1, 1996; 3(6): 445 - 454.
[Abstract] [PDF]


Home page
ScienceHome page
A Rustici, M Velucchi, R Faggioni, M Sironi, P Ghezzi, S Quataert, B Green, and M Porro
Molecular mapping and detoxification of the lipid A binding site by synthetic peptides
Science, January 15, 1993; 259(5093): 361 - 365.
[Abstract] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1989 by the American Society for Investigative Pathology.