Loss of claudin-1 in lipopolysaccharide-treated periodontal epithelium

Authors

  • T. Fujita,

    1. Department of Periodontal Medicine, Divisionof Frontier Medical Science, Hiroshima University Graduate School of Biomedical Sciences, Minami-ku, Hiroshima, Japan
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  • J. D. Firth,

    1. Department of Oral Biological and Medical Sciences, Faculty of Dentistry, University of British Columbia, Vancouver, BC, Canada
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  • M. Kittaka,

    1. Department of Periodontal Medicine, Divisionof Frontier Medical Science, Hiroshima University Graduate School of Biomedical Sciences, Minami-ku, Hiroshima, Japan
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  • D. Ekuni,

    1. Department of Preventive Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Kita-ku, Okayama, Japan
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  • H. Kurihara,

    1. Department of Periodontal Medicine, Divisionof Frontier Medical Science, Hiroshima University Graduate School of Biomedical Sciences, Minami-ku, Hiroshima, Japan
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  • E. E. Putnins

    1. Department of Oral Biological and Medical Sciences, Faculty of Dentistry, University of British Columbia, Vancouver, BC, Canada
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Edward E. Putnins, PhD, DMD, Oral Biological and Medical Sciences, Faculty of Dentistry, The University of British Columbia, 2199 Wesbrook Mall, Vancouver, BC, Canada V6T 1Z3
Tel: +1 604 822 1734
Fax: +1 604 822 3562
e-mail: putnins@dentistry.ubc.ca

Abstract

Fujita T, Firth JD, Kittaka M, Ekuni D, Kurihara H, Putnins EE. Loss of claudin-1 in lipopolysaccharide-treated periodontal epithelium. J Periodont Res 2012; 47: 222–227. © 2011 John Wiley & Sons A/S

Background and Objective:  The epithelial barrier is a critical component of innate immunity and provides protection against microbial invasion. Claudin-1, a tight junction protein, is known to contribute to the epithelial cell barrier. An experimentally induced rat periodontal disease model was used to study the effects of lipopolysaccharide (LPS) on the expression of tight junction-associated molecule genes in the junctional epithelium.

Material and Methods:  LPS was applied for 8 wk in the gingival sulcus, and junctional epithelium was collected by laser-capture microdissection and subjected to microarray analysis.

Results:  Microarray analysis identified that expression of the claudin-1 gene was decreased in the epithelium by chronic LPS challenge. Immunohistochemical analysis confirmed the expression of claudin-1 protein in junctional epithelium and that 8 wk of chronic LPS topical application significantly reduced claudin-1 expression. The effect of LPS on claudin-1 protein expression was validated using a porcine junctional epithelial cell culture Transwell model. The epithelial barrier, as measured using transmembrane resistance, was significantly reduced after 3 wk of LPS challenge and this was associated with a decreased level of expression of claudin-1 protein.

Conclusion:  These results confirm that the initiation of experimental periodontal disease is associated with reduction in the expression of claudin-1 gene and protein. This decreased level of a critical tight junction protein may result in the disruption of barrier function and may play an important role in the initiation of periodontal disease.

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