Porphyromonas gingivalis lipopolysaccharide delays human polymorphonuclear leukocyte apoptosis in vitro.
Apoptosis (programmed cell death) is a mechanism by which superfluous or damaged cells undergo changes that lead to selective removal from organ systems by phagocytic cells. Certain bacterial products delay apoptosis in neutrophils (PMNs). In this study, PMNs were incubated for up to 8 h with varying concentrations of lipopolysaccharide (LPS), lipid A or capsular polysaccharide isolated from 3 strains of Porphyromonas gingivalis (Pg) (strains HG-184, A7A1-28 and 381). Assay runs included controls containing cells and medium but no bacterial products. Fluorescence microscopy was used to evaluate apoptotic changes. PMNs exhibited a time-dependent increase in the number 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 other and to Escherichia coli 0111:B4 LPS. Lipid A from the 3 Pg strains also delayed apoptosis (p < 0.05), but was less potent than LPS or synthetic lipid A. Capsular polysaccharide had no significant effect on apoptosis (p > 0.05). Thus, LPS and lipid A from P. gingivalis appear to modulate the functional lifespan of PMNs. This could potentiate the inflammatory and destructive components of periodontal diseases.
Preshaw
P M
PM
Department of Periodontology, College of Dentistry, Ohio State University, Columbus 43210, USA. preshaw.1@osu.edu
Schifferle
R E
RE
Walters
J D
JD
D017209:Apoptosis / Q000187:drug effects*; D016667:Bacterial Capsules / Q000494:pharmacology; D002470:Cell Survival / Q000187:drug effects; D004305:Dose-Response Relationship, Drug; D004926:Escherichia coli / Q000378:metabolism; D006801:Humans; D008050:Lipid A / Q000494:pharmacology; D008070:Lipopolysaccharides / Q000008:administration & dosage / Q000494:pharmacology*; D008856:Microscopy, Fluorescence; D009504:Neutrophils / Q000187:drug effects*; D010510:Periodontal Diseases / Q000382:microbiology; D010586:Phagocytes / Q000502:physiology; D011135:Polysaccharides, Bacterial / Q000494:pharmacology; D016966:Porphyromonas gingivalis / Q000502:physiology*; D013997:Time Factors
D008050:Lipid A; D008070:Lipopolysaccharides; D011135:Polysaccharides, Bacterial