A Potential Pathogenic Factor from Mycoplasma hominis is a TLR2-Dependent, Macrophage-Activating, P50-Related Adhesin

Authors

  • Akira Hasebe,

    Corresponding author
    1. Division of Rheumatology, Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City, UT, USA
    2. Department of Oral Pathobiological Science, Hokkaido University Graduate School of Dental Medicine, Sapporo, Japan
    • Correspondence

      Akira Hasebe, Department of Oral Pathobiological Science, Hokkaido University Graduate School of Dental Medicine, Kita 13, Nishi 7, Kita-ku, Sapporo 060-8586, Japan. E-mail: akkun@den.hokudai.ac.jp

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  • Hong-Hua Mu,

    1. Division of Rheumatology, Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City, UT, USA
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  • Barry C. Cole

    1. Division of Rheumatology, Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City, UT, USA
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Abstract

Problem

Mycoplasma hominis has been implicated in many inflammatory conditions of the human urogenital tract in particular amniotic infections that lead to fetal and neonatal disease and pre-term labor. The mechanisms responsible are poorly defined.

Method of Study

Biochemical and immunological methods were used to extract, purify, and characterize an inflammatory component present in M. hominis.

Results

We isolated and purified to homogeneity a 40-kDa bioactive lipoprotein from M. hominis that was a potent TLR2-dependent, CD14-independent activator of the human THP-1 macrophage cell line. Homology searches of the N-terminal sequence revealed that 22 of the first 23 residues were identical to those seen for the phase-variable M. hominis p50 adhesin. The truncated P50t lipoprotein importantly retained its adhesive properties for human macrophages.

Conclusion

The unique adhesin/macrophage activator may play a key role in M. hominis infections by triggering an inflammatory cytokine cascade.

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