Journal of Applied Physiology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

J Appl Physiol 90: 90-98, 2001;
8750-7587/01 $5.00
This Article
Right arrow Full Text Free
Right arrow Full Text (PDF) Free
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
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 Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via ISI Web of Science (15)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Hasday, J. D.
Right arrow Articles by Goldblum, S. E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Hasday, J. D.
Right arrow Articles by Goldblum, S. E.
Vol. 90, Issue 1, 90-98, January 2001

Exposure to febrile temperature modifies endothelial cell response to tumor necrosis factor-alpha

Jeffrey D. Hasday1,3,4,5, Douglas Bannerman2, Sirhan Sakarya2, Alan S. Cross2, Ishwar S. Singh1, Deborah Howard4, Beth-Ellen Drysdale4, and Simeon E. Goldblum2,3,4

1 Divisions of Pulmonary and Critical Care Medicine and 2 Infectious Disease, Department of Medicine, University of Maryland School of Medicine, University of Maryland, the 3 Medical and 4 Research Services of the Baltimore Veterans Affairs Medical Center, and the 5 University of Maryland at Baltimore Cytokine Core Laboratory, Baltimore, Maryland 21201

Fever is an important regulator of inflammation that modifies expression and bioactivity of cytokines, including tumor necrosis factor (TNF)-alpha . Pulmonary vascular endothelium is an important target of TNF-alpha during the systemic inflammatory response. In this study, we analyzed the effect of a febrile range temperature (39.5°C) on TNF-alpha -stimulated changes in endothelial barrier function, capacity for neutrophil binding and transendothelial migration (TEM), and cytokine secretion in human pulmonary artery endothelial cells (EC). Permeability for [14C]BSA tracer was increased by treatment with TNF-alpha , and this effect was augmented by incubating EC at 39.5°C. Treating EC with 2.5 U/ml TNF-alpha stimulated an increase in subsequent neutrophil adherence and TEM. Incubating EC at 39.5°C caused a 30% increase in TEM but did not modify the enhancement of neutrophil adherence or TEM by TNF-alpha treatment. Analysis of cytokine expression in EC cultures exposed to TNF-alpha at either 37° or 39.5°C revealed three patterns of temperature and TNF-alpha responsiveness. Granulocyte-macrophage colony stimulating factor (GM-CSF) and interleukin (IL)-8 were not detectable in untreated EC but were increased after TNF-alpha exposure, and this increase was enhanced at 39.5°C. IL-6 expression was also increased with TNF-alpha exposure, but IL-6 expression was lower in 39.5°C EC cultures. Transforming growth factor-beta 1 was constitutively expressed, and its expression was not influenced either by TNF-alpha or exposure to 39.5°C. These data demonstrate that clinically relevant shifts in body temperature might cause important changes in the effects of proinflammatory cytokines on the endothelium.

endothelial cell; paracellular pathway; fever; neutrophils


This article has been cited by other articles:


Home page
 Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
I. Kuwahara, E. P. Lillehoj, W. Lu, I. S. Singh, Y. Isohama, T. Miyata, and K. C. Kim
Neutrophil elastase induces IL-8 gene transcription and protein release through p38/NF-{kappa}B activation via EGFR transactivation in a lung epithelial cell line
Am J Physiol Lung Cell Mol Physiol, September 1, 2006; 291(3): L407 - L416.
[Abstract] [Full Text] [PDF]

Home page
 J. Immunol.Home page
P. Rice, E. Martin, J.-R. He, M. Frank, L. DeTolla, L. Hester, T. O'Neill, C. Manka, I. Benjamin, A. Nagarsekar, et al.
Febrile-Range Hyperthermia Augments Neutrophil Accumulation and Enhances Lung Injury in Experimental Gram-Negative Bacterial Pneumonia
J. Immunol., March 15, 2005; 174(6): 3676 - 3685.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Pathol.Home page
J. D. Hasday, A. Garrison, I. S. Singh, T. Standiford, G. S. Ellis, S. Rao, J.-R. He, P. Rice, M. Frank, S. E. Goldblum, et al.
Febrile-Range Hyperthermia Augments Pulmonary Neutrophil Recruitment and Amplifies Pulmonary Oxygen Toxicity
Am. J. Pathol., June 1, 2003; 162(6): 2005 - 2017.
[Abstract] [Full Text] [PDF]

Home page
 BloodHome page
W. C. Aird
The role of the endothelium in severe sepsis and multiple organ dysfunction syndrome
Blood, May 15, 2003; 101(10): 3765 - 3777.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Respir. Cell Mol. Bio.Home page
K. G. Birukov, A. A. Birukova, S. M. Dudek, A. D. Verin, M. T. Crow, X. Zhan, N. DePaola, and J. G. N. Garcia
Shear Stress-Mediated Cytoskeletal Remodeling and Cortactin Translocation in Pulmonary Endothelial Cells
Am. J. Respir. Cell Mol. Biol., April 1, 2002; 26(4): 453 - 464.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online