The acute inflammatory response in diverse shock states

Carson C. Chow, Gilles Clermont*, Rukmini Kumar, Claudio Lagoa, Zacharia Tawadrous, David Gallo, Binnie Betten, John Bartels, Gregory Constantine, Mitchell P. Fink, Timothy R. Billiar, Yoram Vodovotz

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

163 Scopus citations


A poorly controlled acute inflammatory response can lead to organ dysfunction and death. Severe systemic inflammation can be induced and perpetuated by diverse insults such as the administration of toxic bacterial products (e.g., endotoxin), traumatic injury, and hemorrhage. Here, we probe whether these varied shock states can be explained by a universal inflammatory system that is initiated through different means and, once initiated, follows a course specified by the cellular and molecular mechanisms of the immune and endocrine systems. To examine this question, we developed a mathematical model incorporating major elements of the acute inflammatory response in C57BI/6 mice, using input from experimental data. We found that a single model with different initiators including the autonomic system could describe the response to various insults. This model was able to predict a dose range of endotoxin at which mice would die despite having been calibrated only in nonlethal inflammatory paradigms. These results show that the complex biology of inflammation can be modeled and supports the hypothesis that shock states induced by a range of physiologic challenges could arise from a universal response that is differently initiated and modulated.

Original languageEnglish
Pages (from-to)74-84
Number of pages11
Issue number1
StatePublished - Jul 2005
Externally publishedYes


  • Hemorrhage
  • Inflammation
  • Mathematical modeling
  • Organ dysfunction
  • Shock


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