| Literature DB >> 15374807 |
Fei Ye1, Dirk Foell, Kei-ich Hirono, Thomas Vogl, Chen Rui, Xianyi Yu, Sayaka Watanabe, Kazuhiro Watanabe, Kei-ichiro Uese, Ikuo Hashimoto, Johannes Roth, Fukiko Ichida, Toshio Miyawaki.
Abstract
Neutrophil-derived S100A12 is strongly upregulated during the acute stage of Kawasaki disease and decreases significantly in response to intravenous immune globulin (IVIG) treatment, whereas in nonresponders, serum concentrations increases after initial treatment. Decreased S100A12 expression in neutrophils was detected initially in nonresponders but increased significantly after IVIG treatment, suggesting delayed inflammatory response of neutrophils in nonresponders. Furthermore, in vitro S100A12 secretion increased with tumor necrosis factor-alpha (TNF-alpha) stimulation, whereas intracellular levels were lower in neutrophils with the higher TNF-alpha dose, suggesting intracellular depletion. S100A12 expression in neutrophils appears to reflect responsiveness to IVIG treatment and is possibly involved in the pathophysiology of acute vasculitis.Entities:
Mesh：
Substances：
Year: 2004 PMID： 15374807 DOI： 10.1016/j.amjcard.2004.05.076
Source DB: PubMed Journal: Am J Cardiol ISSN： 0002-9149 Impact factor: 2.778