Related Experiment Video
Updated: Jul 23, 2025

Imaging InlC Secretion to Investigate Cellular Infection by the Bacterial Pathogen Listeria monocytogenes
Published on: September 19, 2013
The Recruitment and Activation of Plasminogen by Bacteria-The Involvement in Chronic Infection Development
Dorota Satala1, Aneta Bednarek1,2, Andrzej Kozik3
1Department of Comparative Biochemistry and Bioanalytics, Faculty of Biochemistry, Biophysics and Biotechnology, Jagiellonian University, 30-387 Kraków, Poland.
Abstract:
The development of infections caused by pathogenic bacteria is largely related to the specific properties of the bacterial cell surface and extracellular hydrolytic activity. Furthermore, a significant role of hijacking of host proteolytic cascades by pathogens during invasion should not be disregarded during consideration of the mechanisms of bacterial virulence. This is the key factor for the pathogen evasion of the host immune response, tissue damage, and pathogen invasiveness at secondary infection sites after initial penetration through tissue barriers. In this review, the mechanisms of bacterial impact on host plasminogen-the precursor of the important plasma serine proteinase, plasmin-are characterized, principally focusing on cell surface exposition of various proteins, responsible for binding of this host (pro)enzyme and its activators or inhibitors, as well as the fibrinolytic system activation tactics exploited by different bacterial species, not only pathogenic, but also selected harmless residents of the human microbiome. Additionally, the involvement of bacterial factors that modulate the process of plasminogen activation and fibrinolysis during periodontitis is also described, providing a remarkable example of a dual use of this host system in the development of chronic diseases.
Insights
Bacteria hijack host proteolysis, particularly plasminogen, for virulence and immune evasion. This review details bacterial strategies impacting fibrinolysis, relevant to infections and chronic diseases like periodontitis.
Area of Science:
- Microbiology
- Biochemistry
- Immunology
Background:
- Bacterial infections rely on cell surface properties and extracellular enzymes.
- Pathogens exploit host proteolytic cascades for virulence and immune evasion.
- Bacterial invasion involves tissue damage and spread to secondary sites.
Purpose of the Study:
- To review bacterial mechanisms impacting host plasminogen and fibrinolysis.
- To focus on bacterial proteins binding plasminogen and its regulators.
- To describe bacterial tactics for activating the fibrinolytic system.
Main Methods:
- Literature review of bacterial interactions with the fibrinolytic system.
- Analysis of bacterial cell surface proteins involved in plasminogen binding.
- Examination of bacterial modulation of plasminogen activators and inhibitors.
Main Results:
- Pathogenic and commensal bacteria utilize diverse strategies to bind and activate plasminogen.
- Bacterial surface proteins are key mediators of fibrinolytic system manipulation.
- Bacterial hijacking of plasminogen facilitates immune evasion and tissue invasion.
- Specific bacterial factors modulate fibrinolysis in periodontitis, illustrating chronic disease involvement.
Conclusions:
- Bacterial manipulation of plasminogen and fibrinolysis is a critical virulence factor.
- Understanding these mechanisms is vital for combating bacterial infections.
- Targeting bacterial interactions with the host fibrinolytic system offers therapeutic potential.
More Related Videos
08:38Using a Bacterial Pathogen to Probe for Cellular and Organismic-level Host Responses
Published on: February 22, 2019
10:59Conditional Knockdown of Gene Expression in Cancer Cell Lines to Study the Recruitment of Monocytes/Macrophages to the Tumor Microenvironment
Published on: November 23, 2017
Related Concept Videos
Clot Retraction and Fibrinolysis
Formation of the Platelet Plug
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...
Urinary Tract Infection II: Pathophysiology
Inflammation
Bacterial Signaling
Gene Regulation in Microbial Communities: Quorum Sensing