Journal
FEMS IMMUNOLOGY AND MEDICAL MICROBIOLOGY
Volume 65, Issue 3, Pages 481-487Publisher
WILEY
DOI: 10.1111/j.1574-695X.2012.00979.x
Keywords
fibrosis; COL1A2 promoter; Escherichia coli; lipopolysaccharide; Toll-like receptor 4
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Funding
- Labour and Welfare Sciences Research Grants [H20-nanchi-ippan-035, H20-shinko-ippan-012, H22-shinko-ippan-008]
- Ministry of Education, Culture, Sports, Science, and Technology of Japan [20591212]
- Grants-in-Aid for Scientific Research [24591491, 20591212, 24791030] Funding Source: KAKEN
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The relationship between bacterial infection and collagen production was investigated using human fibroblasts transfected with the promoter of COL1A2 , which encodes the a1 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.similar to 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.similar to coli, while antibodies against human TLR2 and human transforming growth factor-beta (TGF-beta) receptor type II did not. These results indicate that E.similar to 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.
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