Neutrophils rescue gingival epithelial cells from bacterial-induced apoptosis.
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.
Galicia
Johnah C
JC
University of Louisville School of Dentistry, Louisville, KY 40202, USA.
Benakanakere
Manjunatha R
MR
Stathopoulou
Panagiota G
PG
Kinane
Denis F
DF
D017209:Apoptosis / Q000276:immunology*; D002478:Cells, Cultured; D016207:Cytokines / Q000378:metabolism; D004847:Epithelial Cells / Q000382:microbiology* / Q000473:pathology; D005881:Gingiva / Q000382:microbiology* / Q000473:pathology; D006801:Humans; D007249:Inflammation; D009504:Neutrophils / Q000276:immunology*; D010447:Peptide Hydrolases / Q000378:metabolism; D010510:Periodontal Diseases; D010587:Phagocytosis / Q000276:immunology; D016966:Porphyromonas gingivalis / Q000276:immunology
D016207:Cytokines; D010447:Peptide Hydrolases