Protection against endotoxic shock by bactericidal/permeability-increasing protein in rats.

H Jin; R Yang; S Marsters; A Ashkenazi; S Bunting; M N Marra; R W Scott; J B Baker

doi:10.1172/JCI117877

Department of Cardiovascular Research, Genentech, Inc., South San Francisco, California 94080, USA.

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Department of Cardiovascular Research, Genentech, Inc., South San Francisco, California 94080, USA.

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Department of Cardiovascular Research, Genentech, Inc., South San Francisco, California 94080, USA.

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Department of Cardiovascular Research, Genentech, Inc., South San Francisco, California 94080, USA.

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Department of Cardiovascular Research, Genentech, Inc., South San Francisco, California 94080, USA.

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Department of Cardiovascular Research, Genentech, Inc., South San Francisco, California 94080, USA.

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Department of Cardiovascular Research, Genentech, Inc., South San Francisco, California 94080, USA.

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Department of Cardiovascular Research, Genentech, Inc., South San Francisco, California 94080, USA.

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Published in Volume 95, Issue 4 on April 1, 1995
J Clin Invest. 1995;95(4):1947–1952. https://doi.org/10.1172/JCI117877.
© 1995 The American Society for Clinical Investigation

Published April 1, 1995 - Version history

Bactericidal/permeability-increasing protein (BPI) is a neutrophil primary granule protein that inhibits effects of LPS in vitro. The current study examined the effects of BPI on hemodynamics, mortality, and circulating endotoxin and cytokines in conscious rats with endotoxic shock. Catheters were implanted into the right femoral artery and vein. 1 d later, human recombinant BPI (10 mg/kg) or vehicle was intravenously injected immediately, 30 min, or 2 h after intravenous injection of LPS (7.5 mg/kg). Mean arterial pressure (MAP) and heart rate were monitored and blood was collected before and after injection. BPI given immediately or 30 min after LPS prevented the LPS-induced reduction in MAP at 4-8 h and markedly reduced mortality. BPI given 2 h after LPS injection had no protective effect. BPI treated immediately after LPS reduced the circulating levels of endotoxin and IL-6 but increased the circulating levels of TNF. We propose that BPI exerts its protective effect through a TNF-independent mechanism, by inhibiting endotoxin-stimulated production of IL-6.

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Protection against endotoxic shock by bactericidal/permeability-increasing protein in rats.

H Jin, R Yang, S Marsters, A Ashkenazi, S Bunting, M N Marra, R W Scott, and J B Baker

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Protection against endotoxic shock by bactericidal/permeability-increasing protein in rats.

H Jin, R Yang, S Marsters, A Ashkenazi, S Bunting, M N Marra, R W Scott, and J B Baker

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