Protein Expression Changes in Human Monocytic THP-1 Cells Treated with Lipoteichoic Acid from Lactobacillus plantarum and Staphylococcus aureus
文献类型: 外文期刊
第一作者: Zeng, Ri-Zhong
作者: Zeng, Ri-Zhong;Kim, Han Geun;Kim, Na Ra;Lee, Hae Young;Jung, Bong Jun;Chung, Dae Kyun;Zeng, Ri-Zhong;Kim, Han Geun;Kim, Na Ra;Lee, Hae Young;Jung, Bong Jun;Chung, Dae Kyun;Zeng, Ri-Zhong;Ko, Mi Yeon;Lee, Seung Yeon;Chung, Dae Kyun;Chung, Dae Kyun
作者机构:
关键词: 2-DE;gram-positive bacteria;lipoteichoic acid;proteome analysis;THP-1 cells
期刊名称:MOLECULES AND CELLS ( 影响因子:5.034; 五年影响因子:4.932 )
ISSN: 1016-8478
年卷期: 2010 年 29 卷 6 期
页码:
收录情况: SCI
摘要: Lipoteichoic acid (LTA) from Staphylococcus aureus (aLTA) and from Lactobacillus plantarum LTA (pLTA) are both recognized by Toll-like receptor 2 (TLR2), but cause different stimulatory effects on the innate immune and inflammatory responses, and their underlying cellular mechanisms are unknown. In this study, comparative proteome analysis was performed using two-dimensional gel electrophoresis and mass spectrometry on protein extracts from human monocyte THP-1 cells stimulated with either aLTA or pLTA. Differentially expressed proteins might be involved in innate immunity and inflammation. Cells treated with aLTA and with pLTA showed different protein expression profiles. Of 60 identified proteins, 10 were present only in treated cells (8 in aLTA-treated only, and 2 in pLTA-treated only), 1 protein (IMPDH2) was suppressed by pLTA, and 49 were up- or down-regulated more than three-fold by aLTA- or pLTA- stimulation. Several proteins involved in immunity or inflammation, anti-oxidation, or RNA processing were significantly changed in expression by aLTA- or pLTA-stimulation, including cyclophilin A, HLA-B27, D-dopachrome tautomerase, Mn-SOD, hnRNP-C, PSF and KSRP. These data demonstrated that aLTA and pLTA had different effects on the protein profile of THP-1 cells. Comparison of the proteome alterations will provide candidate biomarkers for further investigation of the immunomodulatory effects of aLTA and pLTA, and the involvement of aLTA in the pathogenesis of Staphylococcus aureus sepsis.
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