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CRITICAL CARE AND TRAUMA

N-Acetyl-Cysteine Attenuates Endotoxin-Induced Adhesion Molecule Expression in Human Whole Blood

Koichiroh Nandate, MD^*, Masanori Ogata, MD, Hitomi Tamura, MD, Takashi Kawasaki, MD, Takeyoshi Sata, MD, and Akio Shigematsu, MD

*Division of Critical and Emergency Care Medicine and Department of Anesthesiology, University of Occupational and Environmental Health, Kitakyushu, Japan

Address correspondence and reprint requests to Masanori Ogata, MD, Department of Anesthesiology, University of Occupational and Environmental Health, 1-1 Iseigaoka, Yahatanishiku, Kitakyushu 807-8555, Japan. Address e-mail to mogata{at}med.uoeh-u.ac.jp.

Leukocyte adhesion to endothelial cells plays a pivotal role in the early stage of endotoxin shock. The attenuation of the leukocyte response to endotoxin may contribute to the prevention of further organ dysfunction. Recent evidence implies that N-acetyl-cysteine (NAC) attenuates endotoxin-induced pathophysiological changes. We investigated the effect of NAC on the expression of CD11b and CD62L in endotoxin-stimulated human whole blood. NAC (>10 mM) significantly inhibited the lipopolysaccharide (LPS)-induced upregulation of CD11b in a concentration-dependent manner. However, NAC did not affect the LPS-induced downregulation of CD62L. We also analyzed the effect of NAC on interleukin-8 (IL-8)-induced expression of CD11b in human whole blood. IL-8 (10 ng/mL) significantly upregulated the expression of CD11b, and the IL-8-induced upregulation was significantly attenuated by NAC (>10 mM) in a dose-dependent manner. We conclude that NAC attenuates the increased expression of CD11b in either LPS or IL-8-stimulated human whole blood.

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