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29 results on '"Si, Feifei"'

6. The Time Option of IVIG Treatment is Associated with IVIG Resistance in Kawasaki Disease in Southwest China

Author

Peng, Yue, primary, Jing, Fengchuan, additional, Liu, Dong, additional, Li, Bin, additional, Xu, Yanxia, additional, Tan, Zhongyou, additional, Chen, Ouyang, additional, Yang, Yanfeng, additional, Si, Feifei, additional, Jiang, Wenliang, additional, Li, Cong, additional, Cheng, Zhenli, additional, Zhou, Xue, additional, Feng, Siqi, additional, Su, Ya, additional, and Yi, Qijian, additional

Published
2024
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28. The relationship between Interleukin-27gene polymorphisms and Kawasaki disease in a population of Chinese children

Author

Si, Feifei, Wu, Yao, Wang, Xianmin, Gao, Fang, Yang, Dan, Liu, Ruixi, and Yi, Qijian

Abstract

AbstractBackgroundKawasaki disease is the leading cause of acquired heart disease in children from developed countries. The Interleukin-6/ Interleukin-12 cytokine family has many members, including the paradoxical anti- and pro-inflammatory Interleukin-27. Recent studies have demonstrated that Interleukin-27 plays a role in immune diseases. Given this, we sought to evaluate the association between Interleukin-27genetic polymorphisms and Kawasaki disease in Chinese children.Methods and resultsInterleukin-27 was genotyped in 100 Kawasaki disease children and 98 healthy children (controls), resulting in the direct sequencing of eight Single-nucleotide Polymorphisms: rs17855750, rs40837, rs26528, rs428253, rs4740, rs4905, rs153109, and rs181206). There were no significant differences in Interleukin-27 genotypes between Kawasaki disease and control groups. Of the eight Single-nucleotide Polymorphisms, there was a significant increase in the risk of Kawasaki disease with coronary arterial lesions in children with the rs17855750 (T>G), rs40837 (A>G), rs4740 (G>A), rs4905 (A>G), rs153109 (T>C), and rs26528 (A>G) Single-nucleotide Polymorphisms. This was particularly true for rs17855750 (T>G), which had a greater frequency in Kawasaki disease children with coronary arterial aneurysm.ConclusionThese findings may be used as risk factors when assessing a child’s likelihood of developing Kawasaki disease, as well as for the development of future therapeutic treatments for Kawasaki disease.

Published
2018
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29. Resistin Enhances Inflammatory Cytokine Production in Coronary Artery Tissues by Activating the NF- κ B Signaling.

Author

Gao F, Si F, Feng S, Yi Q, and Liu R

Subjects
Animals, Arteritis metabolism, Coronary Aneurysm metabolism, Endothelial Cells cytology, Inflammation, Interleukin-1beta metabolism, Lactobacillus metabolism, Matrix Metalloproteinase 9 metabolism, Mice, Mice, Inbred C57BL, Mucocutaneous Lymph Node Syndrome metabolism, Tumor Necrosis Factor-alpha metabolism, Coronary Vessels metabolism, Cytokines metabolism, NF-kappa B metabolism, Resistin metabolism, Signal Transduction
Abstract

Purpose. Kawasaki disease (KD) is a systemic vasculitis and is a leading cause of coronary artery lesions (CALs) in childhood. Our previous study has shown higher levels of serum Resistin in KD patients with coronary aneurysm. This study aimed at examining the association of Resistin with inflammatory cytokine expression in mouse model of coronary arteritis and determining the potential mechanisms. Methods. C57BL/6 mice were injected with Lactobacillus cell wall extract (LCWE) to induce coronary arteritis. The relative levels of Resistin, TNF- α , IL-1 β , and MMP-9 expression and inflammatory infiltrates in the coronary arteries were determined longitudinally by quantitative RT-PCR, ELISA, and histology. The effect of TLR4 and NF- κ B activation on Resistin-induced TNF- α and IL-1 β expression in human coronary artery endothelium cells (HCAECs) was examined by quantitative RT-PCR. Results. Higher levels of Resistin, TNF- α , IL-1 β , and MMP-9 expression were associated with the degrees of inflammatory infiltrates in the coronary artery walls of the LCWE-injected mice. Resistin enhanced TNF- α and IL-1 β expression in HCAECs at 18 or 24 hours after stimulation. Pretreatment with anti-TLR4 attenuated Resistin-enhanced IL-1 β , but not TNF- α , expression and pretreatment with parthenolide or QNZ demolished Resistin-enhanced TNF- α expression in HACECs. Pretreatment with parthenolide, but not QNZ, blocked Resistin-enhanced IL-1 β expression in HCAECs. Conclusion. Resistin may enhance inflammation by cross-talking with TLR4/NF- κ B signaling during the development of coronary arteritis in mice.

Published
2016
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