Detection of human antibodies binding with smooth and rough LPSs from Proteus mirabilis O3 strains S1959, R110, R45

J Gleńska-Olender1,2, K Durlik1, I Konieczna1

  • 1Institute of Biology, Jan Kochanowski University, 25-406, Kielce, Poland.

Antonie Van Leeuwenhoek
|September 11, 2017
PubMed

Insights

Proteus bacteria can cause infections and rheumatoid arthritis (RA). This study found antibodies recognizing Proteus lipopolysaccharide (LPS) in both healthy individuals and RA patients, suggesting a role in molecular mimicry in RA.

Area of Science:

  • Immunology
  • Microbiology
  • Rheumatology

Background:

  • Proteus bacteria are facultative pathogens linked to urinary tract infections, bacteremia, and rheumatoid arthritis (RA).
  • Lipopolysaccharide (LPS) from Proteus species contains epitopes that may cross-react with host antigens.
  • Molecular mimicry is a proposed mechanism in the pathogenesis of RA.

Purpose of the Study:

  • To compare antibody titers against Proteus mirabilis lipopolysaccharide (LPS) in healthy individuals and RA patients.
  • To investigate the presence of antibodies recognizing specific lysine-galacturonic acid epitopes in Proteus LPS.
  • To explore the potential role of anti-LPS antibodies in molecular mimicry in RA.

Main Methods:

  • Enzyme-linked immunosorbent assay (ELISA) was used to quantify antibody titers.
  • LPS from wild-type and mutant strains of Proteus mirabilis (O3) were utilized.
  • Antibodies were analyzed in plasmas from healthy blood donors and sera from RA patients.

Main Results:

  • Antibody titers against Proteus mirabilis LPS increased with age in blood donors.
  • Both healthy individuals and RA patients possessed antibodies against different forms of Proteus O3 LPS (smooth, Ra, and Re types).
  • Antibodies targeting lysine-galacturonic acid epitopes were detected in both groups, with potential implications for RA.

Conclusions:

  • Antibodies against Proteus mirabilis LPS are present in both healthy and RA populations.
  • The detection of these antibodies suggests a potential role for molecular mimicry involving Proteus LPS in the pathogenesis of RA.
  • Further research is warranted to elucidate the precise mechanisms of anti-LPS antibodies in RA development.

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