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Resistance of Yersinia pestis to complement-dependent killing is mediated by the Ail outer membrane protein

Sara Schesser Bartra1, Katie L Styer, Deanna M O'Bryant

  • 1Department of Microbiology and Immunology, University of Miami Miller School of Medicine, Miami, FL 33101, USA.

Infection and Immunity
|November 21, 2007
PubMed

Insights

The Yersinia pestis Ail outer membrane protein is crucial for resisting complement-mediated killing, essential for plague survival in blood and transmission. This protein protects against host immune responses, aiding bacterial pathogenesis.

Area of Science:

  • Microbiology
  • Immunology
  • Bacterial Pathogenesis

Background:

  • Yersinia pestis causes plague and requires survival in blood for transmission.
  • Ail/Lom family outer membrane proteins confer resistance to complement-dependent killing in pathogenic bacteria.
  • Y. pestis encodes four putative Ail/Lom family proteins.

Purpose of the Study:

  • To investigate the role of Y. pestis Ail/Lom family proteins in resistance to complement-mediated killing.
  • To determine the function of the Ail protein in Y. pestis survival and pathogenesis.

Main Methods:

  • Construction of Y. pestis mutants deficient in Ail/Lom family protein expression using lambda Red-mediated recombination.
  • Assessment of bacterial resistance to complement-mediated killing at different temperatures (6, 26, and 37 degrees C).
  • Expression of Ail in Escherichia coli to evaluate its protective effect against complement.

Main Results:

  • The Ail outer membrane protein was essential for Y. pestis resistance to complement-mediated killing at 26 and 37 degrees C.
  • Ail expression was high at 26 and 37 degrees C but absent at 6 degrees C.
  • Expression of Ail in E. coli conferred protection against complement-mediated bacterial killing, while other Y. pestis Ail/Lom proteins did not.

Conclusions:

  • Ail is a key virulence factor for Yersinia pestis, enabling resistance to complement-mediated killing.
  • The Ail protein's expression and function are temperature-dependent, correlating with potential roles in host environments.
  • Further investigation into Ail's role in infection models (mice, C. elegans, fleas) is warranted.

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