scholarly journals Regulation of Toll-like receptor 4-associated MD-2 in intestinal epithelial cells: a comprehensive analysis

2009 ◽  
Vol 16 (2) ◽  
pp. 93-103 ◽  
Author(s):  
Arunan S. Vamadevan ◽  
Masayuki Fukata ◽  
Elizabeth T. Arnold ◽  
Lisa S. Thomas ◽  
David Hsu ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Comprehensive Analysis ◽  
Intestinal Epithelial ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4

M1776 Toll-Like Receptor 4 (TLR4) is a Target of Wnt/β-Catenin Signaling in Intestinal Epithelial Cells (IEC): Implications for Sporadic Colon Cancer

2010 ◽  
Vol 138 (5) ◽  
pp. S-417 ◽  
Author(s):  
Arunan S. Vamadevan ◽  
Masayuki Fukata ◽  
John P. Sotolongo ◽  
Cecilia Espana ◽  
Rebeca Santaolalla ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Sporadic Colon Cancer

scholarly journals Intracellular Recognition of Lipopolysaccharide by Toll-like Receptor 4 in Intestinal Epithelial Cells

2003 ◽  
Vol 198 (8) ◽  
pp. 1225-1235 ◽  
Author(s):  
Mathias W. Hornef ◽  
Birgitta Henriques Normark ◽  
Alain Vandewalle ◽  
Staffan Normark
Keyword(s):  
Epithelial Cells ◽  
Golgi Apparatus ◽  
Intestinal Epithelial Cells ◽  
Adaptor Protein ◽  
Nuclear Factor Κb ◽  
Intestinal Epithelial ◽  
Toll Like Receptor ◽  
Serine Threonine Kinase ◽  
Toll Like Receptor 4 ◽  
Threonine Kinase

Toll-like receptor (TLR)4 has recently been shown to reside in the Golgi apparatus of intestinal crypt epithelial m-ICcl2 cells, colocalizing with internalized lipopolysaccharide (LPS). Here we demonstrate that disruption of the integrity of the Golgi apparatus significantly reduced LPS-mediated nuclear factor κB activation. Also, the TLR4 adaptor protein MyD88 and the serine/threonine kinase IRAK-1 were rapidly recruited to the Golgi apparatus upon stimulation. LPS-mediated activation required lipid raft formation and intact clathrin-dependent internalization. In contrast to macrophages, prevention of ligand internalization by use of LPS-coated beads significantly impaired recognition by epithelial cells. The localization of TLR4 to the Golgi apparatus was abrogated by expression of a genetically modified form of the TLR4 binding chaperone gp96. Thus, our data provide evidence that in contrast to the situation in macrophages, LPS recognition in intestinal epithelial cells may occur in the Golgi apparatus and require LPS internalization.

scholarly journals Gamma Interferon Augments the Intracellular Pathway for Lipopolysaccharide (LPS) Recognition in Human Intestinal Epithelial Cells through Coordinated Up-Regulation of LPS Uptake and Expression of the Intracellular Toll-Like Receptor 4-MD-2 Complex

2003 ◽  
Vol 71 (6) ◽  
pp. 3503-3511 ◽  
Author(s):  
Manabu Suzuki ◽  
Tadakazu Hisamatsu ◽  
Daniel K. Podolsky
Keyword(s):  
Epithelial Cell ◽  
Epithelial Cells ◽  
Cell Lines ◽  
Intestinal Epithelial Cell ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Epithelial Cell Lines ◽  
Ifn Γ

ABSTRACT Although some intestinal epithelial cell lines are known to respond to lipopolysaccharide (LPS), understanding of the relationship between LPS responsiveness and the expression of LPS receptors or factors regulating LPS responsiveness of intestinal epithelial cell lines is incomplete. In this study, we demonstrate that commonly studied human intestinal epithelial cell lines can be classified into at least three different types on the basis of LPS responsiveness, Toll-like receptor-4 (TLR4) expression, and the effects of gamma interferon (IFN-γ) on LPS responsiveness. The first phenotype, which includes the HCT-116 and Caco-2 cell lines, is characterized by relative hyporesponsiveness to LPS and diminished expression of TLR4 protein. In these cells, IFN-γ does not induce LPS responsiveness. The second phenotype, which includes cell line SW480, exhibits a highly LPS-responsive phenotype and surface expression of TLR4 protein even in unprimed conditions. These lines are functionally similar to cells of monocytic lineage. In the third phenotype, which includes the HT-29 and Colo205 cell lines, TLR4 protein is largely present in the cytoplasmic fraction and the cells are hyporesponsive to LPS in an unprimed condition. However, priming of these cells with IFN-γ can induce LPS responsiveness through augmentation of LPS uptake and expression of MD-2 mRNA and intracellular TLR4 proteins. Finally, these findings suggest that the Th1 cytokine IFN-γ modulates LPS responsiveness through several mechanisms in intestinal epithelial cells and that these cells may comprise different subpopulations with distinct roles in innate immune responses.

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