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Yersinia pestis Plasminogen Activator

1
Université de Lille, Inserm, CNRS, CHU Lille, Institut Pasteur de Lille, U1019—UMR9017—CIIL—Center for Infection and Immunity of Lille, F-59000 Lille, France
2
Department of Molecular Medicine and USF Health Byrd Alzheimer’s Research Institute, Morsani College of Medicine, University of South Florida, Tampa, FL 33612, USA
3
Laboratory of New Methods in Biology, Federal Research Center “Pushchino Scientific Center for Biological Research of the Russian Academy of Sciences”, Institute for Biological Instrumentation of the Russian Academy of Sciences, 142290 Pushchino, Moscow Region, Russia
4
Laboratory for Plague Microbiology, State Research Center for Applied Microbiology and Biotechnology, Especially Dangerous Infections Department, 142279 Obolensk, Moscow Region, Russia
*
Authors to whom correspondence should be addressed.
Biomolecules 2020, 10(11), 1554; https://doi.org/10.3390/biom10111554
Received: 23 October 2020 / Revised: 12 November 2020 / Accepted: 12 November 2020 / Published: 14 November 2020
(This article belongs to the Collection Yersinia pestis Biomolecules)
The Gram-negative bacterium Yersinia pestis causes plague, a fatal flea-borne anthropozoonosis, which can progress to aerosol-transmitted pneumonia. Y. pestis overcomes the innate immunity of its host thanks to many pathogenicity factors, including plasminogen activator, Pla. This factor is a broad-spectrum outer membrane protease also acting as adhesin and invasin. Y. pestis uses Pla adhesion and proteolytic capacity to manipulate the fibrinolytic cascade and immune system to produce bacteremia necessary for pathogen transmission via fleabite or aerosols. Because of microevolution, Y. pestis invasiveness has increased significantly after a single amino-acid substitution (I259T) in Pla of one of the oldest Y. pestis phylogenetic groups. This mutation caused a better ability to activate plasminogen. In paradox with its fibrinolytic activity, Pla cleaves and inactivates the tissue factor pathway inhibitor (TFPI), a key inhibitor of the coagulation cascade. This function in the plague remains enigmatic. Pla (or pla) had been used as a specific marker of Y. pestis, but its solitary detection is no longer valid as this gene is present in other species of Enterobacteriaceae. Though recovering hosts generate anti-Pla antibodies, Pla is not a good subunit vaccine. However, its deletion increases the safety of attenuated Y. pestis strains, providing a means to generate a safe live plague vaccine. View Full-Text
Keywords: Yersinia pestis; plasminogen activator; omptin; pathogenicity factor; pathogenesis; plague Yersinia pestis; plasminogen activator; omptin; pathogenicity factor; pathogenesis; plague
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MDPI and ACS Style

Sebbane, F.; Uversky, V.N.; Anisimov, A.P. Yersinia pestis Plasminogen Activator. Biomolecules 2020, 10, 1554. https://doi.org/10.3390/biom10111554

AMA Style

Sebbane F, Uversky VN, Anisimov AP. Yersinia pestis Plasminogen Activator. Biomolecules. 2020; 10(11):1554. https://doi.org/10.3390/biom10111554

Chicago/Turabian Style

Sebbane, Florent, Vladimir N. Uversky, and Andrey P. Anisimov. 2020. "Yersinia pestis Plasminogen Activator" Biomolecules 10, no. 11: 1554. https://doi.org/10.3390/biom10111554

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