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Microbes Infect. 2019 Apr 19. pii: S1286-4579(19)30051-6. doi: 10.1016/j.micinf.2019.04.004. [Epub ahead of print]

Characterizing the role of tissue-type plasminogen activator in a mouse model of Group A streptococcal infection.

Author information

1
Illawarra Health and Medical Research Institute and School of Chemistry and Molecular Bioscience, Molecular Horizons, University of Wollongong, Wollongong, New South Wales, Australia.
2
W. M. Keck Center for Transgene Research, Department of Chemistry and Biochemistry, University of Notre Dame, Notre Dame, IN, United States.
3
School of Chemistry and Molecular Bioscience, Australian Infectious Diseases Research Centre, University of Queensland, St. Lucia, Queensland, Australia.
4
Illawarra Health and Medical Research Institute and School of Chemistry and Molecular Bioscience, Molecular Horizons, University of Wollongong, Wollongong, New South Wales, Australia. Electronic address: martina@uow.edu.au.

Abstract

Plasmin(ogen) acquisition is critical for invasive disease initiation by Streptococcus pyogenes (GAS). Host urokinase plasminogen activator (uPA) plays a role in mediating plasminogen activation for GAS dissemination, however the contribution of tissue-type plasminogen activator (tPA) to GAS virulence is unknown. Using novel tPA-deficient ALBPLG1 mice, our study revealed no difference in mouse survival, bacterial dissemination or the pathology of GAS infection in the absence of tPA in AlbPLG1/tPA-/- mice compared to AlbPLG1 mice. This study suggests that tPA has a limited role in this humanized model of GAS infection, further highlighting the importance of its counterpart uPA in GAS disease.

KEYWORDS:

Animal infection model; Plasminogen; Streptococcus pyogenes; Streptokinase; Tissue-type plasminogen activator (tPA); Urokinase plasminogen activator (uPA)

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