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Updated: Jun 20, 2026
05:31
Purification and Visualization of Lipopolysaccharide from Gram-negative Bacteria by Hot Aqueous-phenol Extraction
Published on: May 28, 2012
Human complement activation by smooth and rough Proteus mirabilis lipopolysaccharides
Wiesław Kaca1, Michał Arabski, Rafał Fudała
1Division of Clinical Bacteriology, Huddinge University Hospital, Karolinska Institute, Huddinge, Sweden.
Archivum Immunologiae Et Therapiae Experimentalis
|August 27, 2009
Summary
Proteus mirabilis lipopolysaccharides (LPSs) fragment human complement C3, regardless of bacterial strain or serum resistance. This C3 fragmentation by Re-type LPS occurs independently of antibodies, highlighting a key immune evasion mechanism.
Area of Science:
- Immunology
- Microbiology
- Biochemistry
Background:
- Proteus mirabilis is implicated in urinary tract infections, bacteremia, and rheumatoid arthritis.
- Previous work demonstrated smooth-form P. mirabilis lipopolysaccharides (LPSs) fragment human complement C3.
- This study investigates C3 conversion by smooth P. mirabilis S1959 and its polysaccharide-truncated LPSs from R mutant strains.
Purpose of the Study:
- To examine the C3 conversion activity of smooth and rough P. mirabilis lipopolysaccharides (LPSs).
- To investigate the role of LPS structure and outer membrane proteins in P. mirabilis serum resistance.
- To determine the complement pathway involved in C3 fragmentation by Re-type LPS.
Main Methods:
- Capture ELISA and crossed immunoelectrophoresis were used to study C3 conversion to C3c.
- Outer membrane proteins were analyzed by discontinuous sodium dodecyl sulfate gel electrophoresis.
- Complement-deficient human serum was utilized to elucidate the classical pathway's role.
Main Results:
- Smooth P. mirabilis S1959 (O3) resisted serum-dependent killing, unlike Ra and Re mutants.
- Exposed core oligosaccharides in R110 LPS did not confer serum resistance.
- Outer membrane protein composition differed significantly between smooth and rough strains, suggesting a role in complement resistance.
Conclusions:
- All tested P. mirabilis LPSs (S1959, R110, R45) fragmented C3 and exposed C3c neo-antigen.
- The Re-type P. mirabilis R45 LPS fragmented C3 via the antibody-independent classical pathway.
- LPS structure and outer membrane proteins contribute to P. mirabilis's resistance to complement-mediated killing.
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