Research article
Enhanced susceptibility to lipopolysaccharide-induced arthritis and endotoxin shock in interleukin-32 alpha transgenic mice through induction of tumor necrosis factor alpha
1 Department of Orthopaedic Surgery, Keio University, 35 Shinanomachi, Shinjuku, Tokyo 160-8582, Japan
2 Department of Pathology, Keio University, 35 Shinanomachi, Shinjuku, Tokyo 160-8582, Japan
3 Department of Applied Chemistry, Faculty of Science and Technology, Keio University, Hiyoshi 3-14-1, Kohoku-ku, Yokohama 223-8522, Japan
Arthritis Research & Therapy 2012, 14:R120 doi:10.1186/ar3850
Published: 21 May 2012Additional files
Additional file 1:
Figure S1. Phosphorylation of IκB and MAPKs stimulated with rIL-32α (100 ng/ml) in RAW 264.7 cells was determined by Western blotting using anti-phospho-IκB, -ERK1/2, -p38, and -JNK antibodies. Phosphorylation of IκB and ERK1/2 were observed and inhibited by their specific inhibitors, while significant phosphorylation of p38 or JNK. was not observed. This data represents one of three independent experiments.
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Additional file 2:
Figure S2. Levels of TNFα and IL-10 were expressed as a proportion to that in control culture media without IL-32α stimulation. Level of TNFαpeaked at 12 h after stimulation with IL-32α and gradually decreased thereafter, while levels IL-10 kept increasing from 24 to 96 h after stimulation. Values are expressed as mean ± SD of triplicate determinations.
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