Date of Award

8-2003

Degree Type

Thesis

Degree Name

MS Biology

Department

Biology

Advisor

Allan Blake

Committee Member

Sulie L. Chang

Keywords

Lipopolysaccharide, Morphine, LPS-induced inflammation

Abstract

Opiate-addicts have been known to show increased susceptibility to bacterial infection. Lipopolysaccharide (LPS), which is a cell wall component in gram-negative bacterial, is a potent stimulator of inflammation. We investigated how treatment with morphine alters LPS-induced inflammatory responses in the rat. Chronic morphine exposure alone elevated serum endotoxin levels. Animals treated with morphine and LPS (250 µglkg) developed hypothermia, decreased mean arterial pressure (MAP), increased plasma thrombin anti-thrombin III (TAT) complex, and approximately 67% exhibited progressive intramicrovascular coagulation. Morphine also enhanced LPS­ induced leukocyte endothelial adhesion (LEA), suppressed leukocyte flux and corticosterone production, and elevated interleukin- I�, tumor necrotic factor-a, and interleukin-6 serum levels. This study presents both the molecular and cellular mechanisms underlying the potentiated LPS-induced inflammation and accelerated progression to septic shock seen with chronic morphine exposure.

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