Accuri C6 Flow Cytometer System
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Published online before print April 23, 2009
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© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.0109003

Received for publication January 3, 2009.
Revised February 13, 2009.
Accepted for publication March 19, 2009.

Article

Neutrophils rescue gingival epithelial cells from bacterial-induced apoptosis

Johnah C. Galicia , Manjunatha R. Benakanakere , Panagiota G. Stathopoulou , and Denis F. Kinane @

Oral Health and Systemic Disease Research Group, University of Louisville School of Dentistry, Louisville, Kentucky, USA

@ To whom correspondence should be addressed. E-mail: dfkina01{at}louisville.edu.


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Abstract

In the pathogenesis of chronic inflammatory periodontal disease, neutrophils are recognized as a major cellular component from the histopathology of the periodontal lesion around teeth and from clinical cases where absence or dysfunction of neutrophils results in major periodontal destruction. Neutrophils are recruited in vast numbers into the gingival crevice during periodontal inflammation, attracted by microbial plaque chemoattractants and chemokines released following microbial perturbation of gingival epithelial cells. Porphyromonas gingivalis, a major periodontopathogen, triggers a vast array of cellular responses in gingival epithelial cells but also induces apoptosis. We demonstrate here that neutrophils, when combined in a P. gingivalis challenge assay of epithelial cells, prevent epithelial cell apoptosis by phagocytosing P. gingivalis and later undergoing apoptosis themselves. By removing P. gingivalis by phagocytosis, neutrophils also protect the host from the harmful effects of its microbial proteases, which degrade inflammatory cytokines and other host molecules.

Key Words: phagocytosis • host defense • human