N-acetyl-cysteine attenuates endotoxin-induced adhesion molecule expression in human whole blood.
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.
Nandate
Koichiroh
K
*Division of Critical and Emergency Care Medicine and †Department of Anesthesiology, University of Occupational and Environmental Health, Kitakyushu, Japan.
Ogata
Masanori
M
Tamura
Hitomi
H
Kawasaki
Takashi
T
Sata
Takeyoshi
T
Shigematsu
Akio
A
D000111:Acetylcysteine / Q000494:pharmacology*; D039481:CD11b Antigen / Q000096:biosynthesis*; D015815:Cell Adhesion Molecules / Q000096:biosynthesis*; D004305:Dose-Response Relationship, Drug; D004731:Endotoxins / Q000494:pharmacology*; D006801:Humans; D016209:Interleukin-8 / Q000494:pharmacology; D019041:L-Selectin / Q000096:biosynthesis; D007962:Leukocytes / Q000378:metabolism
D039481:CD11b Antigen; D015815:Cell Adhesion Molecules; D004731:Endotoxins; D016209:Interleukin-8; D019041:L-Selectin; D000111:Acetylcysteine