Redundant and Cooperative Roles for Yersinia pestis Yop Effectors in the Inhibition of Human Neutrophil Exocytic Responses Revealed by Gain-of-Function Approach

Author:

Pulsifer Amanda R.1ORCID,Vashishta Aruna2,Reeves Shane A.1,Wolfe Jennifer K.3,Palace Samantha G.4ORCID,Proulx Megan K.4ORCID,Goguen Jon4ORCID,Bodduluri Sobha R.15,Haribabu Bodduluri15,Uriarte Silvia M.2,Lawrenz Matthew B.13ORCID

Affiliation:

1. Department of Microbiology and Immunology, University of Louisville School of Medicine, Louisville, Kentucky, USA

2. Department of Medicine, University of Louisville School of Medicine, Louisville, Kentucky, USA

3. Center for Predictive Medicine for Biodefense and Emerging Infectious Diseases, University of Louisville School of Medicine, Louisville, Kentucky, USA

4. Department of Microbiology and Physiology, University of Massachusetts Medical School, Worcester, Massachusetts, USA

5. James Graham Brown Cancer Center, University of Louisville, Louisville, Kentucky, USA

Abstract

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 Y. pestis to create this early noninflammatory environment is in part due to the action of seven Yop effector proteins that are directly injected into host cells via a type 3 secretion system (T3SS).

Funder

Jewish Heritage Fund for Excellence

HHS | NIH | National Institute of Allergy and Infectious Diseases

HHS | NIH | National Institute of General Medical Sciences

University of Louisville

Publisher

American Society for Microbiology

Subject

Infectious Diseases,Immunology,Microbiology,Parasitology

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