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Yersinia lipopolysaccharide is modified by human monocytes
M Wuorela1, S Jalkanen, P Toivanen
1Department of Medical Microbiology, Turku University, Finland.
Infection and Immunity
|December 1, 1993
Summary
Lipopolysaccharide (LPS) from Yersinia bacteria persists within monocytes for days after infection, remaining immunoreactive. This suggests infected phagocytes continuously release LPS, potentially contributing to reactive arthritis pathogenesis.
Area of Science:
- Immunology
- Microbiology
- Rheumatology
Background:
- Reactive arthritis follows infections, often in HLA B27-positive individuals.
- Bacterial lipopolysaccharide (LPS) is found in joint phagocytes of reactive arthritis patients.
- LPS structures are processed but remain immunoreactive in affected joints.
Purpose of the Study:
- To investigate the in vitro degradation and fate of bacterial lipopolysaccharide (LPS).
- To monitor the processing of LPS within monocytes after exposure to Yersinia enterocolitica.
- To understand the role of LPS in the pathogenesis of reactive arthritis.
Main Methods:
- Monocytes from healthy donors were incubated with heat-killed Yersinia enterocolitica O:3.
- Lipopolysaccharide (LPS) fate was monitored using immunofluorescence and immunoblotting.
- LPS processing and modifications were analyzed via SDS-PAGE.
Main Results:
- Both core and O-polysaccharide regions of LPS persisted in monocyte vacuoles and on the plasma membrane for 7 days.
- Structural modifications of LPS were indicated by altered migration properties.
- Intracellular processing of LPS resulted in core epitopes appearing on the monocyte surface.
Conclusions:
- Monocytes retain and process bacterial LPS, with both core and O-polysaccharide structures persisting.
- Processed LPS appears on the monocyte surface, indicating ongoing release into the microenvironment.
- LPS-containing phagocytes may continuously supply membrane-active LPS to joints, contributing to reactive arthritis.