Pro-inflammatory Cytokines Up-regulate MUC1 Gene Expression in Oral Epithelial Cells

The membrane-bound mucin MUC1 is expressed ubiquitously on epithelial surfaces and is thought to provide protection from bacterial and chemical injury. The present study was undertaken to determine whether MUC1 was expressed in cultured oral epithelial cells and whether expression is modulated by pr...

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Bibliographic Details
Published in:Journal of dental research 2003-11, Vol.82 (11), p.883-887
Main Authors: Li, X., Wang, L., Nunes, D.P., Troxler, R.F., Offner, G.D.
Format: Article
Language:English
Subjects:
Blotting, Northern
Blotting, Western
Cytokines - pharmacology
Dentistry
Epithelial Cells - metabolism
Gene Expression Regulation - drug effects
Humans
Inflammation Mediators - pharmacology
Interferon-gamma - pharmacology
Interleukin-1 - pharmacology
KB Cells
Lipopolysaccharides - pharmacology
Mouth Mucosa - metabolism
Mucin-1 - biosynthesis
Mucin-1 - genetics
Mucin-1 - immunology
Polymerase Chain Reaction
Porphyromonas gingivalis - physiology
Recombinant Proteins
RNA, Messenger - biosynthesis
Statistics, Nonparametric
Tumor Necrosis Factor-alpha - pharmacology
Up-Regulation
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Summary:The membrane-bound mucin MUC1 is expressed ubiquitously on epithelial surfaces and is thought to provide protection from bacterial and chemical injury. The present study was undertaken to determine whether MUC1 was expressed in cultured oral epithelial cells and whether expression is modulated by pro-inflammatory mediators released as part of the host response to infection by oral pathogens. Northern and Western blotting experiments showed that KB cells express MUC1 mRNA and protein. When cells were treated with interleukins (IL-1β, IL-6), tumor necrosis factor-alpha (TNF-α), or interferon-gamma (IFN-γ), or combinations of these, real-time PCR demonstrated that MUC1 mRNA increased 1.4- to 3.2-fold. Interestingly, a significant increase in levels of MUC1 protein was also observed. While no effect was observed when KB cells were incubated with LPS from Porphyromonas gingivalis, infection of KB monolayers with this oral pathogen caused a 2.85-fold increase in MUC1 transcript levels. These results suggest that increased MUC1 synthesis may be a key element in the host response to infection with oral pathogens.
ISSN:0022-0345
1544-0591
DOI:10.1177/154405910308201107