Mast cells, which interact with Escherichia coli, up-regulate genes associated with innate immunity and become less responsive to FcεRI-mediated activation

被引:37
作者
Kulka, Marianna
Fukuishi, Nobuyuki
Rottem, Menachem
Mekori, Yoseph A.
Metcalfe, Dean D.
机构
[1] NIAID, NIH, LAD, Bethesda, MD 20892 USA
[2] Northwestern Univ, Feinberg Sch Med, Allergy Immunol Div, Chicago, IL 60611 USA
[3] Tel Aviv Univ, Sackler Sch Med, IL-69978 Tel Aviv, Israel
[4] Meir Hosp, Dept Med, Kefar Sava, Israel
关键词
IgE; MIP-3; beta; CCL-19; CCL-18;
D O I
10.1189/jlb.1004600
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Mast cells, which are associated with T helper cell type 2-dependent inflammation, have now been implicated in the innate immune response. To further characterize how mast cells are programmed to respond to infectious organisms, we used expression profiling using DNA microarray analysis of gene expression by human mast cells (huMC) during ingestion of Escherichia coli and examined immunoglobulin E (IgE)-mediated degranulation. Analysis of data revealed that specific groups of genes were modulated, including genes encoding transcription factors, cell signaling molecules, cell cycle regulators, enzymes, cytokines, novel chemokines of the CC family, adhesion molecules, and costimulatory molecules. Enzyme-linked immunosorbent assay analysis confirmed the production of tumor necrosis factor and the chemokines CC chemokine ligand (CCL)-1/I-309, CCL-19/macrophage-inflammatory protein-3 beta (MIP-3 beta), and CCL-18/MIP-4; flow cytometry confirmed the up-regulation of carcinoembryonic antigen-related cell adhesion molecule 1, the integrin CD49d, and CD80. Coincubation with E. coli down-regulated Fc receptor for IgE I (Fc epsilon RI) expression and Fe epsilon RI-mediated hnMC degranulation. These data are consistent with the concept that bacterial exposure directs mast cell responses toward innate immunity and away from IgE-mediated effects.
引用
收藏
页码:339 / 350
页数:12
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