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Timothy A. Pritts, MD; Quan Wang, MD, PhD; Xiaoyan Sun, MD, PhD; M. Ryan Moon, MD; David R. Fischer, MD; Josef E. Fischer, MD; Hector R. Wong, MD; Per-Olof Hasselgren, MD

Arch Surg. 2000;135:860-866.

Background  Results of previous studies suggest that the stress response protects cells and tissues by regulating proinflammatory mediators. The transcription factor nuclear factor-kappa B (NF-B), normally sequestered in the cytoplasm by its inhibitory protein, IB, regulates many genes involved in inflammatory responses to critical illness. Endotoxemia is associated with increased NF-B activity in intestinal mucosa, but the effect of the stress response on endotoxin-induced NF-B activation in intestinal mucosa is not known.

Hypothesis  Induction of the stress response inhibits NF-B DNA binding activity in jejunal mucosa during endotoxemia.

Methods  The stress response was induced in mice by hyperthermia (42°C) or injection with sodium arsenite (10 mg/kg). After 2 to 5 hours, mice were injected with endotoxin (lipopolysaccharide, 12.5 mg/kg) or a corresponding volume of sterile saline. One hour later, jejunal mucosa was harvested for preparation of nuclear and cytoplasmic extracts.

Results  Mucosal levels of heat shock protein–72 increased after hyperthermia or treatment with sodium arsenite, consistent with induction of the stress response. The increase in NF-B DNA binding activity and decrease in IB- levels seen after endotoxin injection were inhibited by previous induction of the stress response.

Conclusion  The protective effects of the stress response in vivo might, at least in part, be due to inhibited NF-B activation.

From the Departments of Surgery (Drs Pritts, Sun, Moon, D. R. Fischer, J. E. Fischer, and Hasselgren) and Molecular and Cellular Physiology (Dr Pritts), University of Cincinnati, Division of Critical Care, Children's Hospital Medical Center (Dr Wong), Veterans Affairs Medical Center (Dr Hasselgren), and Shriners Hospital for Children (Drs Pritts, Wang, D. R. Fischer, and Hasselgren), Cincinnati, Ohio.

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