Journal Article

Activation of <i>COL1A2</i> promoter in human fibroblasts by <i>Escherichia coli</i>

Haruko Miyazaki, Ryo Kobayashi, Hiroki Ishikawa, Naoki Awano, Satoshi Yamagoe, Yoshitsugu Miyazaki and Tetsuya Matsumoto

in FEMS Immunology & Medical Microbiology

Published on behalf of Federation of Microbiological Societies

Volume 65, issue 3, pages 481-487
Published in print August 2012 | ISSN: 0928-8244
Published online July 2012 | e-ISSN: 1574-695X | DOI: http://dx.doi.org/10.1111/j.1574-695X.2012.00979.x
Activation of COL1A2 promoter in human fibroblasts by Escherichia coli

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Abstract

The relationship between bacterial infection and collagen production was investigated using human fibroblasts transfected with the promoter of COL1A2, which encodes the α1 chain of human type I collagen, linked to a luciferase reporter. The cells were used to assess the gene promoter activity of COL1A2 following bacterial stimulation. The COL1A2 promoter was activated by stimulation with fixed Escherichia coli in a dose-dependent manner, but not by fixed Staphylococcus aureus. Enhancement of collagen production was observed in the E. coli-stimulated fibroblasts compared to those without stimulation. Both anti-human Toll-like receptor (TLR) 4 antibody and polymyxin B clearly blocked the COL1A2 promoter activity stimulated by E. coli, while antibodies against human TLR2 and human transforming growth factor-β (TGF-β) receptor type II did not. These results indicate that E. coli can directly interact with TLR4 expressed on the surface of fibroblasts and can further induce human type I collagen gene expression and collagen production in these cells. These data also suggest that infection by gram-negative bacteria may cause fibrosis.

Keywords: fibrosis; COL1A2 promoter; Escherichia coli; lipopolysaccharide; Toll-like receptor 4

Journal Article.  3673 words.  Illustrated.

Subjects: Medical Microbiology and Virology ; Biotechnology ; Genetics and Genomics ; Microbiology ; Molecular and Cell Biology

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