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Vol. 126 No. 1, January 1991 |
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PAPERS READ BEFORE THE TENTH ANNUAL MEETING OF THE SURGICAL INFECTION SOCIETY, CINCINNATI, OHIO, June 15, 1990-PART I |
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Interferon-gamma Reverses Bone Marrow Inhibition Following Hemorrhagic Shock
David H. Livingston, MD
Arch Surg. 1991;126(1):100-103.
Abstract
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Hemorrhagic shock has been demonstrated to alter the myelopoietic response to bacterial lipopolysaccharide. Interferongamma has been shown to improve the immune response following experimental shock and injury; however, its effect on myelopoiesis is controversial. This study was performed to determine whether treatment with interferon-gamma will improve the bone marrow response to lipopolysaccharide after hemorrhagic shock. Rats subjected to either shock or a sham procedure were allocated into three groups: (1) control rats received no further treatment; (2) lipopolysaccharide-treated rats received saline for 3 days and then were challenged with lipopolysaccharide to stimulate myelopoiesis; and (3) interferon-treated rats received interferon-gamma (7500 U subcutaneously 1 hour after shock and then every day for 3 days) and lipopolysaccharide as in group 2. Serum colony-stimulating factor levels were measured 6 hours and bone marrow white blood cell count and granulocyte-macrophage colony-forming units (CFU-GM) were measured 24 hours following lipopolysaccharide administration. In sham-treated rats, lipopolysaccharide increased CFU-GM 77% compared with controls. In contrast, treatment with lipopolysaccharide decreased CFU-GM 43% following shock. Treatment with interferon-gamma increased CFU-GM in all animals and reversed the decline in CFU-GM seen in shocked lipopolysaccharide-treated animals. Serum colony-stimulating factor levels were unaffected by either shock or interferon-gamma administration. These data demonstrate that interferon-gamma exerts a stimulatory effect on bone marrow following shock and restores the myelopoietic response to lipopolysaccharide.
(Arch Surg. 1991;126:100-103)
Author Affiliations
From the Department of Surgery, University of Medicine and Dentistry–New Jersey Medical School, Newark.
Footnotes
Accepted for publication October 14, 1990.
Read before the Tenth Anniversary Meeting of the Surgical Infection Society, Cincinnati, Ohio, June 16, 1990.
Reprint requests to University Hospital C-384, 150 Bergen St, Newark, NJ 07103 (Dr Livingston).
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