Inhibition of lipopolysaccharide stimulated interleukin-1beta production after subarachnoid hemorrhage

• Published in: Neurological research (New York) Vol. 29; no. 1; p. 47
• Main Authors: Kinoshita, Kosaku, Yamaguchi, Junko, Sakurai, Atsushi, Ebihara, Takayuki, Furukawa, Makoto, Tanjoh, Katsuhisa
• Format: Journal Article
• Language: English
• Published: England 01.01.2007
• Subjects: Adult; Biomarkers - blood; Catecholamines - blood; Catecholamines - pharmacology; Cells, Cultured; Dopamine - blood; Down-Regulation - drug effects; Down-Regulation - immunology; Encephalitis - blood; Encephalitis - immunology; Encephalitis - physiopathology; Epinephrine - blood; Female; Humans; Interleukin-10 - blood; Interleukin-1beta - blood; Interleukin-1beta - secretion; Leukocytes, Mononuclear - drug effects; Leukocytes, Mononuclear - immunology; Leukocytes, Mononuclear - secretion; Lipopolysaccharides - pharmacology; Male; Middle Aged; Subarachnoid Hemorrhage - complications; Subarachnoid Hemorrhage - immunology; Subarachnoid Hemorrhage - physiopathology; Tumor Necrosis Factor-alpha - blood; Up-Regulation - drug effects; Up-Regulation - immunology
• ISSN: 0161-6412

To identify the characteristics of cytokine production from peripheral blood mononuclear cells (PBMCs) in response to lipopolysaccharide (LPS) in patients with subarachnoid hemorrhage (SAH). Blood samples were collected on the first day and 3 days after SAH (n = 12) to measure plasma concentrations of catecholamines, tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1beta and IL-10. PBMCs from SAH patients or healthy volunteers were incubated with LPS (1 microg) for 24 hours. In the second phase, PBMCs from healthy volunteers (n = 6) were incubated with or without catecholamine (10 micromol/1) for 6 hours. After pre-treatment, the cells were treated with LPS (1 microg) for 18 hours. Supernatants were extracted and subjected to measurement by enzyme-linked immunosorbent assay. Plasma concentrations of epinephrine or dopamine prolong increased significantly 3 days after SAH, involved in elevation of plasma IL-10. In the PBMCs from the SAH patients, LPS-stimulated IL- 10 production was inhibited significantly. Pre-treatment with epinephrine or dopamine inhibited LPS-stimulated IL-1beta production significantly in the PBMCs from the healthy volunteers. The initial SAH involved in an impaired production of pro-inflammatory cytokines in response to LPS with an elevation of plasma epinephrine, dopamine and IL-10 after acute stressful conditions. This phenomenon may play an important role of an early immnosupression in patients with poor grade SAH.