Title

Induction of system xc- in mouse bone marrow-derived macrophages by bacterial ligands

Presenter Information

Kristina Finsaas

Presentation Type

Poster

Abstract

The two main types of inflammatory bowel disease (IBD), Crohn?s Disease (CD) and Ulcerative Colitis (UC), affect millions of people worldwide. Expression of the amino acid antiporter, system xc-, is elevated on macrophages in the inflamed mucosa of UC and CD patients, as well as in mouse models of IBD. The goal of this project was to determine the differential regulation of system xc- by macrophages in response to bacterial ligands in vitro. We hypothesized that interaction between intestinal bacterial flora and macrophages via toll like receptor (TLR) activation results in enhanced system xc- expression and macrophage activation. To test this hypothesis, we quantified the expression of system xc- in bone marrow macrophages in response to the model bacterial TLR ligand, LPS, acting through TLR4. We measured system xc- mRNA using RT-PCR and system xc- protein expression using flow cytometry and immunoblotting. We defined the potency of this TLR ligand to upregulate system xc- activity using radioactive amino acids. Finally, we examined molecular mechanisms that regulate system xc- expression on macrophages using recombinant mouse interleukin 10 and the NF-kappa B signaling inhibitor, SN-50. The results from this study will broaden our understanding of system xc- in intestinal homeostasis and disease.

This document is currently not available here.

Share

COinS
 
Apr 13th, 11:00 AM Apr 13th, 12:00 PM

Induction of system xc- in mouse bone marrow-derived macrophages by bacterial ligands

UC Ballroom

The two main types of inflammatory bowel disease (IBD), Crohn?s Disease (CD) and Ulcerative Colitis (UC), affect millions of people worldwide. Expression of the amino acid antiporter, system xc-, is elevated on macrophages in the inflamed mucosa of UC and CD patients, as well as in mouse models of IBD. The goal of this project was to determine the differential regulation of system xc- by macrophages in response to bacterial ligands in vitro. We hypothesized that interaction between intestinal bacterial flora and macrophages via toll like receptor (TLR) activation results in enhanced system xc- expression and macrophage activation. To test this hypothesis, we quantified the expression of system xc- in bone marrow macrophages in response to the model bacterial TLR ligand, LPS, acting through TLR4. We measured system xc- mRNA using RT-PCR and system xc- protein expression using flow cytometry and immunoblotting. We defined the potency of this TLR ligand to upregulate system xc- activity using radioactive amino acids. Finally, we examined molecular mechanisms that regulate system xc- expression on macrophages using recombinant mouse interleukin 10 and the NF-kappa B signaling inhibitor, SN-50. The results from this study will broaden our understanding of system xc- in intestinal homeostasis and disease.