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Group B streptococcus (GBS) modifies macrophage phosphatidylserine metabolism during induction of apoptosis
Sandra Buratta1, Katia Fettucciari, Raffaela Mambrini
1Department of Internal Medicine, Biochemistry Section, University of Perugia, 06122 Perugia, Italy.
Abstract:
Group B streptococcus (GBS) induced macrophage apoptosis by which it could avoid host defence mechanisms. Macrophages, which constitutively express phosphatidylserine (PtdSer) on the outer leaflet of plasma membrane, increased PtdSer exposure during GBS-induced apoptosis. Induction of apoptosis decreased PtdSer radioactivity of macrophages incubated with [(3)H]serine. The effect appeared not due to increasing conversion of PtdSer to phosphatidylethanolamine or phosphatidylcholine nor to the release of radioactive membrane vesicles. The radioactivity in lysoPtdSer was also reduced. These results confirm that induction of apoptosis involves a modification of PtdSer metabolism and point out the typical features of the GBS-induced apoptosis with respect to other models of apoptosis.
Insights
Group B streptococcus (GBS) triggers macrophage apoptosis to evade immune defenses. This process alters phosphatidylserine (PtdSer) metabolism and increases its external exposure on apoptotic cells.
Area of Science:
- Microbiology
- Immunology
- Cell Biology
Background:
- Group B streptococcus (GBS) is a significant pathogen that can evade host immune responses.
- Macrophages play a crucial role in innate immunity and are targeted by pathogens.
- Phosphatidylserine (PtdSer) exposure on the cell surface is a hallmark of apoptosis.
Purpose of the Study:
- To investigate the mechanism by which GBS induces macrophage apoptosis.
- To characterize the changes in phosphatidylserine (PtdSer) metabolism during GBS-induced apoptosis.
- To compare GBS-induced apoptosis with other models of programmed cell death.
Main Methods:
- Macrophages were incubated with Group B streptococcus (GBS).
- Apoptosis induction was assessed.
- Phosphatidylserine (PtdSer) exposure and metabolism were analyzed using radiolabeled serine.
- Changes in PtdSer conversion to phosphatidylethanolamine and phosphatidylcholine were evaluated.
- Release of radioactive membrane vesicles was measured.
Main Results:
- GBS successfully induced macrophage apoptosis.
- Apoptosis led to increased phosphatidylserine (PtdSer) exposure on the macrophage plasma membrane.
- Incubation with radiolabeled serine showed decreased PtdSer radioactivity in apoptotic macrophages.
- This reduction was not due to increased conversion to other phospholipids or vesicle release.
- Radioactivity in lysoPtdSer was also diminished.
Conclusions:
- GBS-induced apoptosis involves significant modifications in phosphatidylserine (PtdSer) metabolism.
- Increased PtdSer exposure during GBS-induced apoptosis is a key feature of this pathogen's immune evasion strategy.
- The observed metabolic alterations in PtdSer distinguish GBS-induced apoptosis from other apoptotic models.