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Cancer Cell death Cell cycle Cytoskeleton Exo/endocytosis Differentiation Division Organelles Signalling Stem cells Trafficking
Cell Biology International (2010) 34, S74 (Printed in Great Britain)
Meeting Abstract
Antiflammin-1 enhanced IL-10 gene expression and secretion in activated macrophages challenged by LPS
Tianjie ZHANG12, Jianzhong HAN1, Chen LI1, Yu Chen1, Jiangping XU1, Dandan FENG1, Huijun Liu1, Yanghong HUANG1 and Ziqiang LUO1*
1Department of Physiology, Xiangya School of Medicine,Central South University, Changhsha, Hunan, China, and 2Department of Physiology, Xiangnan University, Chenzhou, Hunan, China


Antiflammin-1 (MQMKKVLDS, AF-1) is a potent anti-inflammatory nonpeptide, with equivalent sequence to the 9 C-terminal amino acid recidue of α-helix 3 of uteroglobin. But the anti-inflammatory mechanism of AF-1 is still unclear. Interleukin-10 is a potent anti-inflammatory and immune regulatory cytokine, Alveolar macrophages are important host defence cells and one of the important sources of IL-10 in the lung. This research investigated the effect of AF-1 on LPS induced IL-10 production and gene expression in RAW264.7 cells in order to elucidate its possible anti-inflammatory mechanism. Results showed that IL-10 expression and secretion in RAW264.7 cells challenged by LPS (1 µg/ml) was increased in time dependent way, with ultimate peak at 24h (p<0.01). AF-1 (100μmol/L) alone had no effect on IL-10 mRNA expression and secretion in RAW264.7 cells (p>0.05). However, AF-1 (1-100 μmol/L) increased IL-10 mRNA expression and secretion in activated RAW264.7 cells challenged by LPS in a dose- and time- dependent way (p<0.05 and p<0.01). Pretreatment with anti-uteroglobin-binding protein (UGBP) antibody could attenuate the enhanced effect of AF-1 on LPS induced IL-10 gene expression in macrophages. Conclusion: AF-1 could significantly increased IL-10 mRNA expressions and secretion in RAW264.7 cells induced by LPS, the increased effect of AF-1 on LPS induced IL-10 gene expression and secretion in macrophages was mediated by UGBP. The work was supported by the National Natural Science Foundation of China (No. 30670770, 30870916).


*correspondence author



Published online 1 August 2010, doi:10.1042/CBI034S074a


© The Author(s) Journal compilation © 2010 Portland Press Limited


ISSN Print: 1065-6995
ISSN Electronic: 1095-8355
Published by Portland Press Limited on behalf of the International Federation for Cell Biology (IFCB)