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Porphyromonas gingivalis lipopolysaccharide delays human polymorphonuclear leukocyte apoptosis in vitro
P M Preshaw1, R E Schifferle, J D Walters
1Department of Periodontology, College of Dentistry, Ohio State University, Columbus 43210, USA. preshaw.1@osu.edu
Abstract:
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.
Insights
Lipopolysaccharide and lipid A from Porphyromonas gingivalis delay programmed cell death in neutrophils (PMNs). This bacterial modulation of PMN lifespan may worsen periodontal disease inflammation and destruction.
Area of Science:
- Immunology
- Microbiology
- Cell Biology
Background:
- Apoptosis, or programmed cell death, is crucial for removing damaged cells.
- Neutrophils (PMNs) are key immune cells involved in fighting infections.
- Bacterial products can interfere with normal cellular processes like apoptosis.
Purpose of the Study:
- To investigate the effect of Porphyromonas gingivalis (Pg) components on neutrophil apoptosis.
- To determine if lipopolysaccharide (LPS), lipid A, or capsular polysaccharide from Pg influences PMN lifespan.
Main Methods:
- Neutrophils (PMNs) were incubated with varying concentrations of Pg LPS, lipid A, and capsular polysaccharide.
- Apoptotic changes were assessed using fluorescence microscopy over an 8-hour period.
- Statistical analysis was performed to determine significance (p < 0.05).
Main Results:
- Pg lipopolysaccharide (LPS) significantly delayed PMN apoptosis in a dose-dependent manner.
- Lipid A from Pg also delayed apoptosis but was less potent than LPS.
- Capsular polysaccharide from Pg had no significant effect on PMN apoptosis.
Conclusions:
- Pg LPS and lipid A modulate the functional lifespan of neutrophils.
- This modulation may contribute to the inflammatory and destructive processes in periodontal diseases.
- Understanding these mechanisms can inform strategies for managing periodontal conditions.