Open AccessRequirement for Intercellular Adhesion Molecule 1 and Caveolae in Invasion of Human Oral Epithelial Cells by Porphyromonas gingivalis
Author(s) -
Riyoko Tamai,
Yasuyuki Asai,
Tomohiko Ogawa
Publication year - 2005
Publication title -
infection and immunity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.508
H-Index - 220
eISSN - 1070-6313
pISSN - 0019-9567
DOI - 10.1128/iai.73.10.6290-6298.2005
Subject(s) - porphyromonas gingivalis , biology , intercellular adhesion molecule 1 , caveolae , colocalization , cell adhesion molecule , microbiology and biotechnology , signal transduction , bacteria , genetics
Porphyromonas gingivalis , a periodontopathic bacterium, is known to invade oral epithelial cells in periodontal lesions, although the mechanism is unclear. In the present study, goat polyclonal anti-intercellular adhesion molecule 1 (anti-ICAM-1) antibody inhibited the invasion ofP. gingivalis into KB cells (human oral epithelial cells). Further, theP. gingivalis fimbria, a pathogenic adhesion molecule, bound to recombinant human ICAM-1, as shown by enzyme-linked immunosorbent assay.P. gingivalis was also found to colocalize with ICAM-1 on KB cells, as seen with an immunofluorescence microscope, and the knockdown of ICAM-1 in KB cells resulted in the inhibition ofP. gingivalis invasion by RNA interference. In addition, methyl-β-cyclodextrin, a cholesterol-binding agent, inhibited the colocalization ofP. gingivalis with ICAM-1 and invasion by the microorganism. The colocalization of caveolin-1, a caveolar marker protein, on KB cells withP. gingivalis was also shown, and the knockdown of caveolin-1 in KB cells caused a reduced level ofP. gingivalis invasion. These results suggest that ICAM-1 and caveolae are required for the invasion ofP. gingivalis into human oral epithelial cells, and these molecules appear to be associated with the primary stages of the development and progression of chronic periodontitis.