science pharmaceutical expo biotech jobs
Originally published online as doi:10.1189/jlb.0303108 on August 1, 2003

Published online before print August 1, 2003
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
jlb.0303108v1
74/5/916    most recent
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 arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Grutkoski, P. S.
Right arrow Articles by Ayala, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Grutkoski, P. S.
Right arrow Articles by Ayala, A.
(Journal of Leukocyte Biology. 2003;74:916-922.)
© 2003 by Society for Leukocyte Biology

Sepsis-induced SOCS-3 expression is immunologically restricted to phagocytes

P. S. Grutkoski, Y. Chen, C. S. Chung and A. Ayala1

Division of Surgical Research, Rhode Island Hospital and Brown University Medical School, Providence

1Correspondence: Division of Surgical Research, Aldrich 227, Rhode Island Hospital, 593 Eddy Street, Providence, RI 02903. E-mail: aayala{at}lifespan.org

We have shown that immune cells from septic mice exhibit a suppressed response to exogenous stimuli in vitro. The suppressors of the cytokine signaling (SOCS) family are proteins that block intracellular signaling and can be induced by inflammatory mediators. Therefore, we hypothesized that SOCS-3 is up-regulated in immune cells in response to a septic challenge induced by cecal ligation and puncture (CLP). Mice were subjected to CLP or sham-CLP, and 2–48 h later, the blood, thymus, spleen, lung, and peritoneal leukocytes were harvested and examined. SOCS-3 was undetectable in thymocytes or blood leukocytes. In contrast, SOCS-3 was up-regulated in the spleen, lung, and peritoneal leukocytes in a time-dependent manner. Further examination revealed that only the macrophages and neutrophils expressed SOCS-3. These data suggest that cytokines and bacterial toxins present during sepsis have the ability to suppress the cytokine and/or lipopolysaccharide response and the function of immune cells by up-regulating SOCS-3.

Key Words: macrophage • neutrophil • immunosuppression • CLP • mouse




This article has been cited by other articles:


Home page
 J. Immunol.Home page
C. van 't Veer, P. S. van den Pangaart, M. A. D. van Zoelen, M. de Kruif, R. S. Birjmohun, E. S. Stroes, A. F. de Vos, and T. van der Poll
Induction of IRAK-M Is Associated with Lipopolysaccharide Tolerance in a Human Endotoxemia Model
J. Immunol., November 15, 2007; 179(10): 7110 - 7120.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Pathol.Home page
D. E. Wesche-Soldato, C.-S. Chung, S. H. Gregory, T. P. Salazar-Mather, C. A. Ayala, and A. Ayala
CD8+ T Cells Promote Inflammation and Apoptosis in the Liver after Sepsis: Role of Fas-FasL
Am. J. Pathol., July 1, 2007; 171(1): 87 - 96.
[Abstract] [Full Text] [PDF]

Home page
 BloodHome page
D. E. Wesche-Soldato, C.-S. Chung, J. Lomas-Neira, L. A. Doughty, S. H. Gregory, and A. Ayala
In vivo delivery of caspase-8 or Fas siRNA improves the survival of septic mice
Blood, October 1, 2005; 106(7): 2295 - 2301.
[Abstract] [Full Text] [PDF]