IAI FigSearch
Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
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 arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by O'Brien, D. P.
Right arrow Articles by Nahm, M. H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by O'Brien, D. P.
Right arrow Articles by Nahm, M. H.

 Previous Article  |  Next Article 

Infection and Immunity, February 1999, p. 595-601, Vol. 67, No. 2
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Tumor Necrosis Factor Alpha Receptor I Is Important for Survival from Streptococcus pneumoniae Infections

David P. O'Brien,1 David E. Briles,2 Alexander J. Szalai,2 Anh-Hue Tu,2 Inaki Sanz,3 and Moon H. Nahm1,4,*

Departments of Pediatrics,1 Medicine,3 and Pathology,4 University of Rochester School of Medicine and Dentistry, Rochester, New York 14642, and Department of Microbiology, University of Alabama at Birmingham, Birmingham, Alabama 352942

Received 23 July 1998/Returned for modification 3 September 1998/Accepted 4 November 1998

Tumor necrosis factor alpha (TNF-alpha ) is important in resistance to various microorganisms and provides signals to the target cells through two different receptors, TNF-alpha receptor I (TNFRI) (p55 receptor) and TNFRII (p75 receptor). To delineate the significance of the two different signaling pathways in resisting infections with extracellular bacteria, we examined the resistance of mice to Streptococcus pneumoniae (serotype 6B). TNF-alpha needs to be present early in infections, since one injection of wild-type mice with anti-TNF-alpha leads to an increased susceptibility of these mice to S. pneumoniae. TNF-alpha signaling through the p55 receptor (but not the p75 receptor) is crucial in resisting S. pneumoniae infections, because intraperitoneal injection of 100 CFU/mouse killed p55-deficient mice by day 2 of infection, whereas 1,000,000 CFU/mouse was needed to kill half of the control mice. p55-deficient mice do not show evidence of a deficient acute-phase response. All three types of mice (p55 deficient, p75 deficient, and normal) showed comparable rises in the levels of two acute-phase proteins (serum amyloid P and C3) at 24, 48, and 72 h after the experimental infections, and all of the mice showed comparable influxes of neutrophils to the site of infection. Finally, it was demonstrated that p55-deficient mice can be protected from the lethal effects of S. pneumoniae infection by injection of antibodies specific for S. pneumoniae polysaccharide capsule.

* Corresponding author. Mailing address: University of Rochester School of Medicine, 601 Elmwood Ave., Box 777, Rochester, NY 14642. Phone: (716) 275-7963. Fax: (716) 271-7512. E-mail: moon{at}vaccine.rochester.edu.

Infection and Immunity, February 1999, p. 595-601, Vol. 67, No. 2
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


This article has been cited by other articles:



Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
J. Bacteriol. J. Virol. Eukaryot. Cell
Microbiol. Mol. Biol. Rev. Clin. Vaccine Immunol. All ASM Journals

Copyright © 1999 by the American Society for Microbiology. All rights reserved.