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.
journal_name
J Leukoc Bioljournal_title
Journal of leukocyte biologyauthors
Galicia JC,Benakanakere MR,Stathopoulou PG,Kinane DFdoi
10.1189/jlb.0109003subject
Has Abstractpub_date
2009-07-01 00:00:00pages
181-6issue
1eissn
0741-5400issn
1938-3673pii
jlb.0109003journal_volume
86pub_type
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