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Role of the Yersinia pestis Ail Protein in Preventing a Protective Polymorphonuclear Leukocyte Response during Bubonic Plague

Role of the Yersinia pestis Ail Protein in Preventing a Protective Polymorphonuclear Leukocyte... Role of the Yersinia pestis Ail Protein in Preventing a Protective Polymorphonuclear Leukocyte Response during Bubonic Plague ▿ B. Joseph Hinnebusch 1 , * , Clayton O. Jarrett 1 , Julie A. Callison 1 , Donald Gardner 2 , Susan K. Buchanan 3 and Gregory V. Plano 4 1 Laboratory of Zoonotic Pathogens 2 Veterinary Pathology Section, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana 59840 3 Laboratory of Molecular Biology, National Institute of Diabetes & Digestive & Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892 4 Department of Microbiology and Immunology, University of Miami Miller School of Medicine, Miami, Florida 33101 J. B. Bliska , Editor ABSTRACT The ability of Yersinia pestis to forestall the mammalian innate immune response is a fundamental aspect of plague pathogenesis. In this study, we examined the effect of Ail, a 17-kDa outer membrane protein that protects Y. pestis against complement-mediated lysis, on bubonic plague pathogenesis in mice and rats. The Y. pestis ail mutant was attenuated for virulence in both rodent models. The attenuation was greater in rats than in mice, which correlates with the ability of normal rat serum, but not mouse serum, to kill ail -negative Y. pestis in vitro . Intradermal infection with the ail mutant resulted in an atypical, subacute form of bubonic plague associated with extensive recruitment of polymorphonuclear leukocytes (PMN or neutrophils) to the site of infection in the draining lymph node and the formation of large purulent abscesses that contained the bacteria. Systemic spread and mortality were greatly attenuated, however, and a productive adaptive immune response was generated after high-dose challenge, as evidenced by high serum antibody levels against Y. pestis F1 antigen. The Y. pestis Ail protein is an important bubonic plague virulence factor that inhibits the innate immune response, in particular the recruitment of a protective PMN response to the infected lymph node. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Infection and Immunity American Society For Microbiology

Role of the Yersinia pestis Ail Protein in Preventing a Protective Polymorphonuclear Leukocyte Response during Bubonic Plague

Role of the Yersinia pestis Ail Protein in Preventing a Protective Polymorphonuclear Leukocyte Response during Bubonic Plague

Infection and Immunity , Volume 79 (12): 4984 – Dec 1, 2011

Abstract

Role of the Yersinia pestis Ail Protein in Preventing a Protective Polymorphonuclear Leukocyte Response during Bubonic Plague ▿ B. Joseph Hinnebusch 1 , * , Clayton O. Jarrett 1 , Julie A. Callison 1 , Donald Gardner 2 , Susan K. Buchanan 3 and Gregory V. Plano 4 1 Laboratory of Zoonotic Pathogens 2 Veterinary Pathology Section, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana 59840 3 Laboratory of Molecular Biology, National Institute of Diabetes & Digestive & Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892 4 Department of Microbiology and Immunology, University of Miami Miller School of Medicine, Miami, Florida 33101 J. B. Bliska , Editor ABSTRACT The ability of Yersinia pestis to forestall the mammalian innate immune response is a fundamental aspect of plague pathogenesis. In this study, we examined the effect of Ail, a 17-kDa outer membrane protein that protects Y. pestis against complement-mediated lysis, on bubonic plague pathogenesis in mice and rats. The Y. pestis ail mutant was attenuated for virulence in both rodent models. The attenuation was greater in rats than in mice, which correlates with the ability of normal rat serum, but not mouse serum, to kill ail -negative Y. pestis in vitro . Intradermal infection with the ail mutant resulted in an atypical, subacute form of bubonic plague associated with extensive recruitment of polymorphonuclear leukocytes (PMN or neutrophils) to the site of infection in the draining lymph node and the formation of large purulent abscesses that contained the bacteria. Systemic spread and mortality were greatly attenuated, however, and a productive adaptive immune response was generated after high-dose challenge, as evidenced by high serum antibody levels against Y. pestis F1 antigen. The Y. pestis Ail protein is an important bubonic plague virulence factor that inhibits the innate immune response, in particular the recruitment of a protective PMN response to the infected lymph node.

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References (47)

Publisher
American Society For Microbiology
Copyright
Copyright © 2011 by the American society for Microbiology.
ISSN
0019-9567
eISSN
1098-5522
DOI
10.1128/IAI.05307-11
pmid
21969002
Publisher site
See Article on Publisher Site

Abstract

Role of the Yersinia pestis Ail Protein in Preventing a Protective Polymorphonuclear Leukocyte Response during Bubonic Plague ▿ B. Joseph Hinnebusch 1 , * , Clayton O. Jarrett 1 , Julie A. Callison 1 , Donald Gardner 2 , Susan K. Buchanan 3 and Gregory V. Plano 4 1 Laboratory of Zoonotic Pathogens 2 Veterinary Pathology Section, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana 59840 3 Laboratory of Molecular Biology, National Institute of Diabetes & Digestive & Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892 4 Department of Microbiology and Immunology, University of Miami Miller School of Medicine, Miami, Florida 33101 J. B. Bliska , Editor ABSTRACT The ability of Yersinia pestis to forestall the mammalian innate immune response is a fundamental aspect of plague pathogenesis. In this study, we examined the effect of Ail, a 17-kDa outer membrane protein that protects Y. pestis against complement-mediated lysis, on bubonic plague pathogenesis in mice and rats. The Y. pestis ail mutant was attenuated for virulence in both rodent models. The attenuation was greater in rats than in mice, which correlates with the ability of normal rat serum, but not mouse serum, to kill ail -negative Y. pestis in vitro . Intradermal infection with the ail mutant resulted in an atypical, subacute form of bubonic plague associated with extensive recruitment of polymorphonuclear leukocytes (PMN or neutrophils) to the site of infection in the draining lymph node and the formation of large purulent abscesses that contained the bacteria. Systemic spread and mortality were greatly attenuated, however, and a productive adaptive immune response was generated after high-dose challenge, as evidenced by high serum antibody levels against Y. pestis F1 antigen. The Y. pestis Ail protein is an important bubonic plague virulence factor that inhibits the innate immune response, in particular the recruitment of a protective PMN response to the infected lymph node.

Journal

Infection and ImmunityAmerican Society For Microbiology

Published: Dec 1, 2011

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