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Staphylococci are responsible for many infections in humans, starting with skin and soft tissue infections and finishing with invasive diseases such as endocarditis, sepsis and pneumonia, which lead to high mortality. Patients with sepsis often demonstrate activated clotting pathways, decreased levels of anticoagulants, decreased fibrinolysis, activated endothelial surfaces and activated platelets. This results in disseminated intravascular coagulation and formation of a microthrombus, which can lead to a multiorgan failure. This review describes various staphylococcal virulence factors that contribute to vascular thrombosis, including deep vein thrombosis in infected patients. The article presents mechanisms of action of different factors released by bacteria in various host defense lines, which in turn can lead to formation of blood clots in the vessels.
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http://dx.doi.org/10.1016/j.micres.2024.127703 | DOI Listing |
Med Int (Lond)
August 2025
Department of Epidemiology, School of Public Health, Zhengzhou University, Zhengzhou, Henan 450001, P.R. China.
Punicalagin, a polyphenolic compound extracted from pomegranate peel, has received increasing attention in recent years due to its antibacterial and antiviral properties. Punicalagin is capable of inhibiting bacterial growth at sub-inhibitory concentrations by affecting cell membrane formation, disrupting membrane integrity, altering cell permeability, affecting efflux pumps, interfering with quorum sensing and influencing virulence factors. Additionally, punicalagin inhibits viruses by modulating enzyme activity, interacting with viral surface proteins, affecting gene expression, blocking viral attachment, disrupting virus receptor interaction and inhibiting viral replication.
View Article and Find Full Text PDFBiochem Pharmacol
September 2025
Key Laboratory of Artificial Organs and Computational Medicine in Zhejiang Province, Institute of Translational Medicine, Zhejiang Shuren University, 310015 Hangzhou, China. Electronic address:
Methicillin-resistant Staphylococcus aureus (MRSA) is a highly virulent and drug-resistant pathogen frequently causing bacterial pneumonia. Currently, there are limited effective treatments available due to the rapidly evolving resistance of bacteria. Therefore, there is an urgent need to develop novel therapies that focus on host-pathogen interactions.
View Article and Find Full Text PDFCrit Rev Immunol
September 2025
Department of Pharmacy, Birla Institute of Technology and Science (BITS) Pilani, Hyderabad Campus, Dist. Medchal,500078, Telangana State, India.
Caseinolytic protease P (ClpP) is a highly conserved serine protease that plays a pivotal role in protein homeostasis and quality control in bacteria, mitochondria of mammalian cells, and plant chloroplasts. As the proteolytic core of the ATP-dependent Clp protease complex, ClpP partners with regulatory ATPases (e.g.
View Article and Find Full Text PDFmBio
September 2025
Department of Microbiology, Howard Taylor Ricketts Laboratory, The University of Chicago, Lemont, Illinois, USA.
infection is a frequent cause of sepsis in humans, a disease associated with high mortality and without specific intervention. Clumping factor A (ClfA) displayed on the bacterial surface plays a key role in promoting replication during invasive disease. Decades of research have pointed to a wide array of ligands engaged by ClfA.
View Article and Find Full Text PDFmBio
September 2025
The Lundquist Institute for Biomedical Innovation at Harbor-UCLA Medical Center, Torrance, California, USA.
Unlabelled: Methicillin-resistant (MRSA) is a leading cause of endovascular infections, where interactions with endothelial cells play a critical role in pathogenesis. Gp05, a prophage-encoded protein, has previously been implicated in promoting antibiotic persistence by modulating MRSA cellular physiology and evading neutrophil-mediated killing. In this study, we investigated the role of Gp05 in MRSA-endothelial cell interactions, focusing on its impact on bacterial adhesion, invasion, cytotoxicity, and the host inflammatory response.
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