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Arthropathic properties of cell wall polymers from normal flora bacteria
Infection and Immunity
|January 1, 1986
Summary
Bacterial peptidoglycan-polysaccharide (PG-PS) fragments from normal flora and pathogenic bacteria can induce arthritis in rats. Different PG-PS structures cause varying degrees of acute and chronic joint inflammation.
Area of Science:
- Microbiology
- Immunology
- Rheumatology
Background:
- Bacterial cell walls contain peptidoglycan-polysaccharide (PG-PS) structures.
- The role of PG-PS from various bacteria in inducing joint inflammation is not fully understood.
Purpose of the Study:
- To investigate the arthritogenic potential of PG-PS fragments from different bacterial species.
- To compare the inflammatory responses induced by PG-PS from group A and D streptococci, normal flora, and archaeal pseudomurein-PS.
Main Methods:
- Purification of PG-PS and pseudomurein-PS fragments from bacterial cell walls, minimizing autolytic activity.
- Intraarticular and intraperitoneal injection of purified fragments into rats to induce arthritis.
- Assessment of acute and chronic joint inflammation and disease progression.
Main Results:
- All tested PG-PS fragments induced acute inflammation upon intraarticular injection.
- Intraperitoneal injection revealed varying arthritic responses: group D streptococcal PG-PS induced severe acute arthritis evolving into chronic disease that subsided by 60 days.
- Group A streptococcal PG-PS induced severe acute arthritis progressing to chronic erosive joint disease active after 128 days.
- PG-PS from normal flora bacteria (P. acnes, Peptostreptococcus productus) induced a spectrum of acute and chronic arthritis.
- Pseudomurein-PS fragments showed significantly lower or no arthritic activity, highlighting the importance of the PG moiety.
Conclusions:
- Bacterial PG-PS structures are potent inducers of arthritis in a rat model.
- The specific structure of PG-PS determines the severity and chronicity of the induced joint disease.
- Normal flora bacteria possess PG-PS with the potential to cause a range of arthritic conditions, from transient acute inflammation to chronic erosive joint disease.