Neutrophils rescue gingival epithelial cells from bacterial-induced apoptosis
AUTOR(ES)
Galicia, Johnah C.
FONTE
The Society for Leukocyte Biology
RESUMO
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.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2704621Documentos Relacionados
- Activation of liver X receptors and retinoid X receptors prevents bacterial-induced macrophage apoptosis
- Human Gingival Fibroblasts Rescue Butyric Acid-Induced T-Cell Apoptosis
- Inactivation of Mycobacterium tuberculosis mannosyltransferase pimB reduces the cell wall lipoarabinomannan and lipomannan content and increases the rate of bacterial-induced human macrophage cell death
- Dietary antioxidants protect gut epithelial cells from oxidant-induced apoptosis
- Apoptosis of human intestinal epithelial cells after bacterial invasion.