Porphyromonas gingivalis lipopolysaccharide delays human polymorphonuclearleukocyte apoptosis in vitro

Citation
Pm. Preshaw et al., Porphyromonas gingivalis lipopolysaccharide delays human polymorphonuclearleukocyte apoptosis in vitro, J PERIOD RE, 34(4), 1999, pp. 197-202
Citations number
22
Categorie Soggetti
da verificare
Journal title
JOURNAL OF PERIODONTAL RESEARCH
ISSN journal
00223484 → ACNP
Volume
34
Issue
4
Year of publication
1999
Pages
197 - 202
Database
ISI
SICI code
0022-3484(199905)34:4<197:PGLDHP>2.0.ZU;2-U
Abstract
Apoptosis (programmed cell death) is a mechanism by which superfluous or da maged cells undergo changes that lead to selective removal from organ syste ms by phagocytic cells. Certain bacterial products delay apoptosis in neutr ophils (PMNs). In this study, PMNs were incubated for up to 8 h with varyin g concentrations of lipopolysaccharide (LPS), lipid A or capsular polysacch aride isolated from 3 strains of Porphyromonas gingivalis (Pg) (strains HG- 184, A7A1-28 and 381). Assay runs included controls containing cells and me dium but no bacterial products. Fluorescence :microscopy was used to evalua te apoptotic changes. PMNs exhibited a time-dependent increase in the numbe r of apoptotic cells. When cells were cultured in the presence of LPS from any of the 3 Pg strains, apoptosis was delayed in a dose-dependent fashion (p < 0.05). The effects of these LPS preparations were similar to each othe r and to Escherichia coli O111:B4 LPS. Lipid A from the 3 Pg strains also d elayed apoptosis (p < 0.05), but was less potent than LPS or synthetic lipi d A. Capsular polysaccharide had no significant effect on apoptosis (p > 0. 05). Thus, LPS and lipid A from P. gingivalis appear to modulate the functi onal lifespan of PMNs. This could potentiate the inflammatory and destructi ve components of periodontal diseases.