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Role of the Yersinia pestis Ail protein in preventing a protective polymorphonuclear leukocyte response during

B Joseph Hinnebusch1, Clayton O Jarrett, Julie A Callison

  • 1Laboratory of Zoonotic Pathogens, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana 59840, USA. jhinnebusch@niaid.nih.gov

Infection and Immunity
|October 5, 2011
PubMed

Insights

The Yersinia pestis Ail protein hinders the innate immune response, impacting bubonic plague. Deleting the Ail gene in Y. pestis reduces virulence and alters the immune cell response in infected lymph nodes.

Area of Science:

  • Microbiology
  • Immunology
  • Pathogenesis

Background:

  • Yersinia pestis causes plague by evading the host's innate immune system.
  • The outer membrane protein Ail (17-kDa) confers resistance to complement-mediated lysis.
  • Understanding Ail's role is crucial for dissecting plague pathogenesis.

Purpose of the Study:

  • To investigate the impact of the Y. pestis Ail protein on bubonic plague pathogenesis in mouse and rat models.
  • To determine if Ail influences the innate immune response, specifically polymorphonuclear leukocyte (PMN) recruitment.

Main Methods:

  • Generation and characterization of a Y. pestis ail mutant.
  • Intradermal infection of mice and rats with wild-type and ail mutant strains.
  • Assessment of bacterial virulence, dissemination, mortality, and host immune cell infiltration (PMNs).
  • In vitro serum bactericidal assays using mouse and rat serum.

Main Results:

  • The Y. pestis ail mutant exhibited significantly attenuated virulence in both mice and rats, with greater attenuation in rats.
  • Rat serum demonstrated potent bactericidal activity against the ail mutant, unlike mouse serum.
  • Infection with the ail mutant led to subacute plague with extensive PMN recruitment and abscess formation in lymph nodes, but reduced systemic spread and mortality.
  • A robust adaptive immune response, indicated by high anti-F1 antibody levels, was generated after high-dose challenge with the ail mutant.

Conclusions:

  • The Y. pestis Ail protein is a key virulence factor essential for overcoming the host's innate immune defenses during bubonic plague.
  • Ail inhibits the protective polymorphonuclear leukocyte (PMN) response, particularly PMN recruitment to the infected lymph node.
  • Targeting Ail may represent a strategy to attenuate Y. pestis virulence and enhance host immune responses.

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