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Infection and Immunity, February 2008, p. 612-622, Vol. 76, No. 2
0019-9567/08/$08.00+0     doi:10.1128/IAI.01125-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Resistance of Yersinia pestis to Complement-Dependent Killing Is Mediated by the Ail Outer Membrane Protein{triangledown}

Sara Schesser Bartra,1,5 Katie L. Styer,2 Deanna M. O'Bryant,3 Matthew L. Nilles,3 B. Joseph Hinnebusch,4 Alejandro Aballay,2 and Gregory V. Plano1*

Department of Microbiology and Immunology, University of Miami Miller School of Medicine, Miami, Florida 33101,1 Department of Molecular Genetics and Microbiology, Duke University Medical Center, Durham, North Carolina 27710,2 Department of Microbiology and Immunology, University of North Dakota School of Medicine and Health Sciences, Grand Forks, North Dakota 58202,3 Laboratory of Zoonotic Pathogens, Rocky Mountain Laboratories, NIH, NIAID, Hamilton, Montana 59840,4 Department of Molecular Biology, Umeå University, 901 87 Umeå, Sweden5

Received 13 August 2007/ Returned for modification 11 September 2007/ Accepted 30 October 2007

Yersinia pestis, the causative agent of plague, must survive in blood in order to cause disease and to be transmitted from host to host by fleas. Members of the Ail/Lom family of outer membrane proteins provide protection from complement-dependent killing for a number of pathogenic bacteria. The Y. pestis KIM genome is predicted to encode four Ail/Lom family proteins. Y. pestis mutants specifically deficient in expression of each of these proteins were constructed using lambda Red-mediated recombination. The Ail outer membrane protein was essential for Y. pestis to resist complement-mediated killing at 26 and 37°C. Ail was expressed at high levels at both 26 and 37°C, but not at 6°C. Expression of Ail in Escherichia coli provided protection from the bactericidal activity of complement. High-level expression of the three other Y. pestis Ail/Lom family proteins (the y1682, y2034, and y2446 proteins) provided no protection against complement-mediated bacterial killing. A Y. pestis ail deletion mutant was rapidly killed by sera obtained from all mammals tested except mouse serum. The role of Ail in infection of mice, Caenorhabditis elegans, and fleas was investigated.

* Corresponding author. Mailing address: Department of Microbiology and Immunology, University of Miami Miller School of Medicine, Miami, FL 33101. Phone: (305) 243-6310. Fax: (305) 243-4623. E-mail: gplano{at}med.miami.edu

{triangledown} Published ahead of print on 19 November 2007.

Editor: A. J. Bäumler

Infection and Immunity, February 2008, p. 612-622, Vol. 76, No. 2
0019-9567/08/$08.00+0     doi:10.1128/IAI.01125-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



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