Journal of Leukocyte Biology eBioscience full spectrum cell analysis
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Originally published online as doi:10.1189/jlb.0607377 on November 5, 2007

Published online before print November 5, 2007
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
jlb.0607377v1
83/3/553    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
Google Scholar
Right arrow Articles by Lowry, S. F.
Right arrow Articles by Calvano, S. E.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Lowry, S. F.
Right arrow Articles by Calvano, S. E.
(Journal of Leukocyte Biology. 2008;83:553-557.)
© 2008 by Society for Leukocyte Biology

Challenges for modeling and interpreting the complex biology of severe injury and inflammation

Stephen F. Lowry1 and Steve E. Calvano

Division of Surgical Sciences, Department of Surgery, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, New Brunswick, New Jersey, USA

1Correspondence: Department of Surgery, UMDNJ, Robert Wood Johnson Medical School, 125 Paterson Street, Suite 7300, New Brunswick, NJ 08901, USA. E-mail: lowrysf{at}umdnj.edu

ABSTRACT

Human injury is associated with inflammatory responses that are modulated by the acute and chronic activity of endogenous factors and exogenous interventions. A characteristic feature of chronic, severe inflammatory states is the diminished signal output variability of many organ systems, including innate immune responsiveness and endogenous neural and endocrine-mediated functions. The attenuation of signal/response variability and integration of feedback capacity may contribute to systemic and tissue-specific deterioration of function. Some well-intentioned therapies directed toward support of systemic and tissue functions may actually promote the loss of system(s) adaptability and contribute to adverse outcomes in severely stressed patients. In vivo and in silico models of stress, injury, and infection have yet to fully define the influences of ongoing stressful stimulae as well as genetic variation and epigenetic factors in the context of an evolving inflammatory state. Experimental and human models incorporating variable, antecedent stress(es) and altered neuroendocrine rhythms might approximate the altered adaptability in immune and organ function responses. Such models may also provide insights into the salient mechanisms of risk and outcome more precisely than do the constrained study conditions of current animal or human models of systemic inflammation.

Key Words: systems biology • endotoxin • heart rate variability






HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2008 by the Society for Leukocyte Biology.