Skip to main content
  • ASM
    • Antimicrobial Agents and Chemotherapy
    • Applied and Environmental Microbiology
    • Clinical Microbiology Reviews
    • Clinical and Vaccine Immunology
    • EcoSal Plus
    • Eukaryotic Cell
    • Infection and Immunity
    • Journal of Bacteriology
    • Journal of Clinical Microbiology
    • Journal of Microbiology & Biology Education
    • Journal of Virology
    • mBio
    • Microbiology and Molecular Biology Reviews
    • Microbiology Resource Announcements
    • Microbiology Spectrum
    • Molecular and Cellular Biology
    • mSphere
    • mSystems
  • Log in
  • My alerts
  • My Cart

Main menu

  • Home
  • Articles
    • Current Issue
    • Accepted Manuscripts
    • Archive
    • Minireviews
  • For Authors
    • Submit a Manuscript
    • Scope
    • Editorial Policy
    • Submission, Review, & Publication Processes
    • Organization and Format
    • Errata, Author Corrections, Retractions
    • Illustrations and Tables
    • Nomenclature
    • Abbreviations and Conventions
    • Publication Fees
    • Ethics Resources and Policies
  • About the Journal
    • About IAI
    • Editor in Chief
    • Editorial Board
    • For Reviewers
    • For the Media
    • For Librarians
    • For Advertisers
    • Alerts
    • RSS
    • FAQ
  • Subscribe
    • Members
    • Institutions
  • ASM
    • Antimicrobial Agents and Chemotherapy
    • Applied and Environmental Microbiology
    • Clinical Microbiology Reviews
    • Clinical and Vaccine Immunology
    • EcoSal Plus
    • Eukaryotic Cell
    • Infection and Immunity
    • Journal of Bacteriology
    • Journal of Clinical Microbiology
    • Journal of Microbiology & Biology Education
    • Journal of Virology
    • mBio
    • Microbiology and Molecular Biology Reviews
    • Microbiology Resource Announcements
    • Microbiology Spectrum
    • Molecular and Cellular Biology
    • mSphere
    • mSystems

User menu

  • Log in
  • My alerts
  • My Cart

Search

  • Advanced search
Infection and Immunity
publisher-logosite-logo

Advanced Search

  • Home
  • Articles
    • Current Issue
    • Accepted Manuscripts
    • Archive
    • Minireviews
  • For Authors
    • Submit a Manuscript
    • Scope
    • Editorial Policy
    • Submission, Review, & Publication Processes
    • Organization and Format
    • Errata, Author Corrections, Retractions
    • Illustrations and Tables
    • Nomenclature
    • Abbreviations and Conventions
    • Publication Fees
    • Ethics Resources and Policies
  • About the Journal
    • About IAI
    • Editor in Chief
    • Editorial Board
    • For Reviewers
    • For the Media
    • For Librarians
    • For Advertisers
    • Alerts
    • RSS
    • FAQ
  • Subscribe
    • Members
    • Institutions

Yersinia pestis

  • Modification of the Pulmonary MyD88 Inflammatory Response Underlies the Role of the <span class="named-content genus-species" id="named-content-1">Yersinia pestis</span> Pigmentation Locus in Primary Pneumonic Plague
    Host Response and Inflammation
    Modification of the Pulmonary MyD88 Inflammatory Response Underlies the Role of the Yersinia pestis Pigmentation Locus in Primary Pneumonic Plague

    Pneumonic plague, caused by Yersinia pestis, is a rapidly progressing bronchopneumonia involving focal bacterial growth, neutrophilic congestion, and alveolar necrosis. Within a short time after inhalation of Y. pestis, inflammatory cytokines are expressed via the Toll/interleukin-1 (IL-1) adaptor...

    Rachel M. Olson, Miqdad O. Dhariwala, William J. Mitchell, Jerod A. Skyberg, Deborah M. Anderson
  • Open Access
    The <span class="named-content genus-species" id="named-content-1">Yersinia pestis</span> GTPase BipA Promotes Pathogenesis of Primary Pneumonic Plague
    Molecular Pathogenesis
    The Yersinia pestis GTPase BipA Promotes Pathogenesis of Primary Pneumonic Plague

    Yersinia pestis is a highly virulent pathogen and the causative agent of bubonic, septicemic, and pneumonic plague. Primary pneumonic plague caused by inhalation of respiratory droplets contaminated with Y. pestis is nearly 100% lethal within 4 to 7 days without antibiotic intervention.

    ...
    Samantha D. Crane, Srijon K. Banerjee, Kara R. Eichelberger, Richard C. Kurten, William E. Goldman, Roger D. Pechous
  • Antibody Opsonization Enhances Early Interactions between <span class="named-content genus-species" id="named-content-1">Yersinia pestis</span> and Neutrophils in the Skin and Draining Lymph Node in a Mouse Model of Bubonic Plague
    Microbial Immunity and Vaccines
    Antibody Opsonization Enhances Early Interactions between Yersinia pestis and Neutrophils in the Skin and Draining Lymph Node in a Mouse Model of Bubonic Plague

    Bubonic plague results when Yersinia pestis is deposited in the skin via the bite of an infected flea. Bacteria then traffic to the draining lymph node (dLN) where they replicate to large numbers. Without treatment, this infection can result in highly fatal septicemia. Several plague vaccine candidates are currently at various stages of development, but no licensed...

    Jeffrey G. Shannon, B. Joseph Hinnebusch
  • Difference in Strain Pathogenicity of Septicemic <span class="named-content genus-species" id="named-content-1">Yersinia pestis</span> Infection in a TLR2<sup>−/−</sup> Mouse Model
    Host Response and Inflammation
    Difference in Strain Pathogenicity of Septicemic Yersinia pestis Infection in a TLR2−/− Mouse Model

    Yersinia pestis is the causative agent of bubonic, pneumonic, and septicemic plague. We demonstrate that Toll-like receptor 2-deficient (TLR2−/−) mice are resistant to septicemic infection by the KIM5 strain of Y. pestis but not to infection by the CO92 Δpgm strain. This...

    Kyle L. O’Donnell, Peter L. Knopick, Riley Larsen, Sanghita Sarkar, Matthew L. Nilles, David S. Bradley
  • Redundant and Cooperative Roles for <span class="named-content genus-species" id="named-content-1">Yersinia pestis</span> Yop Effectors in the Inhibition of Human Neutrophil Exocytic Responses Revealed by Gain-of-Function Approach
    Bacterial Infections
    Redundant and Cooperative Roles for Yersinia pestis Yop Effectors in the Inhibition of Human Neutrophil Exocytic Responses Revealed by Gain-of-Function Approach

    Yersinia pestis causes a rapid, lethal disease referred to as plague. Y. pestis actively inhibits the innate immune system to generate a noninflammatory environment during early stages of infection to promote colonization. The ability of...

    Amanda R. Pulsifer, Aruna Vashishta, Shane A. Reeves, Jennifer K. Wolfe, Samantha G. Palace, Megan K. Proulx, Jon Goguen, Sobha R. Bodduluri, Bodduluri Haribabu, Silvia M. Uriarte, Matthew B. Lawrenz
  • Open Access
    Modeling Pneumonic Plague in Human Precision-Cut Lung Slices Highlights a Role for the Plasminogen Activator Protease in Facilitating Type 3 Secretion
    Molecular Pathogenesis
    Modeling Pneumonic Plague in Human Precision-Cut Lung Slices Highlights a Role for the Plasminogen Activator Protease in Facilitating Type 3 Secretion

    Pneumonic plague is the deadliest form of disease caused by Yersinia pestis. Key to the progression of infection is the activity of the plasminogen activator protease Pla. Deletion of Pla results in a decreased Y. pestis bacterial burden in the lung and failure to progress into the lethal...

    Srijon K. Banerjee, Samantha D. Huckuntod, Shalynn D. Mills, Richard C. Kurten, Roger D. Pechous
  • <em>Yersinia pestis</em> Pla Protein Thwarts T Cell Defense against Plague
    Host Response and Inflammation
    Yersinia pestis Pla Protein Thwarts T Cell Defense against Plague

    Plague is a rapidly lethal human disease caused by the bacterium Yersinia pestis. This study demonstrated that the Y. pestis plasminogen activator Pla, a protease that promotes fibrin degradation, thwarts T cell-mediated defense against fully virulent...

    Stephen T. Smiley, Frank M. Szaba, Lawrence W. Kummer, Debra K. Duso, Jr-Shiuan Lin
  • Open Access
    <span class="named-content genus-species" id="named-content-1">Yersinia pestis</span> Exploits Early Activation of MyD88 for Growth in the Lungs during Pneumonic Plague
    Host Response and Inflammation
    Yersinia pestis Exploits Early Activation of MyD88 for Growth in the Lungs during Pneumonic Plague

    Yersinia pestis causes bubonic, pneumonic, and septicemic plague. Although no longer responsible for pandemic outbreaks, pneumonic plague continues to be a challenge for medical treatment and has been classified as a reemerging disease in some parts of the world.

    Rachel M. Olson, Miqdad O. Dhariwala, William J. Mitchell, Deborah M. Anderson
  • Cellular Microbiology: Pathogen-Host Cell Molecular Interactions
    Gain-of-Function Analysis Reveals Important Virulence Roles for the Yersinia pestis Type III Secretion System Effectors YopJ, YopT, and YpkA

    Virulence of Yersinia pestis in mammals requires the type III secretion system, which delivers seven effector proteins into the cytoplasm of host cells to undermine immune responses. All seven of these effectors are conserved across Y. pestis strains, but three, YopJ, YopT, and YpkA, are apparently...

    Samantha G. Palace, Megan K. Proulx, Rose L. Szabady, Jon D. Goguen
  • Bacterial Infections
    Protein Acetylation Mediated by YfiQ and CobB Is Involved in the Virulence and Stress Response of Yersinia pestis
    Wanbing Liu, Yafang Tan, Shiyang Cao, Haihong Zhao, Haihong Fang, Xiaoyan Yang, Tong Wang, Yazhou Zhou, Yanfeng Yan, Yanping Han, Yajun Song, Yujing Bi, Xiaoyi Wang, Ruifu Yang, Zongmin Du

Pages

  • Next
  • 1
  • 2
  • 3
  • 4
  • 5
  • 6
  • 7
  • 8
  • 9
  • …
  • 12
Back to top

About

  • About IAI
  • Editor in Chief
  • Editorial Board
  • Policies
  • For Reviewers
  • For the Media
  • For Librarians
  • For Advertisers
  • Alerts
  • RSS
  • FAQ
  • Permissions
  • Journal Announcements

Authors

  • ASM Author Center
  • Submit a Manuscript
  • Article Types
  • Ethics
  • Contact Us

Follow #IAIjournal

@ASMicrobiology

       

ASM Journals

ASM journals are the most prominent publications in the field, delivering up-to-date and authoritative coverage of both basic and clinical microbiology.

About ASM | Contact Us | Press Room

 

ASM is a member of

Scientific Society Publisher Alliance

 

American Society for Microbiology
1752 N St. NW
Washington, DC 20036
Phone: (202) 737-3600

Copyright © 2021 American Society for Microbiology | Privacy Policy | Website feedback

Print ISSN: 0019-9567; Online ISSN: 1098-5522