ArticleHaematologica2020
The contact system proteases play disparate roles in streptococcal sepsis.
Article in Haematologica, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- Bacterial factors required for biofilm formation inFrontiers in cellular and infection microbiology · 2026Article
- An antibody targeting high-molecular-weight kininogen blocks contact system activation in a model of polymicrobial sepsis.Journal of thrombosis and haemostasis : JTH · 2025Article
- Multi-omics driven biomarker discovery and pathological insights into Pseudomonas aeruginosa pneumonia.BMC infectious diseases · 2025Article
- Tranexamic acid inhibits group A streptococci-mediated fibrinolysisFrontiers in immunology · 2025Article
- The role of TLR4/MyD88/NF-κB in the protective effect of ulinastatin on the intestinal mucosal barrier in mice with sepsis.BMC anesthesiology · 2023Article
- The contact system in liver injury.Seminars in immunopathology · 2021Review
- The Diagnostic Value of FeTherapeutics and clinical risk management · 2021Article
- Kinins and Their Receptors in Infectious Diseases.Pharmaceuticals (Basel, Switzerland) · 2020Review
- Kininogen supports inflammation and bacterial spreading during Streptococccus Pyogenes Sepsis.EBioMedicine · 2020Article
- Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis causes an activation of the human contact system, an inflammatory response mechanism against foreign surfaces, proteins and pathogens. The serine proteases of the contact system, factor XII and plasma kallikrein, are decreased in plasma of septic patients, which was previously associated with an unfavorable outcome. However, the precise mechanisms and roles of contact system factors in bacterial sepsis are poorly understood. We, therefore, studied the physiological relevance of factor XII and plasma kallikrein in a mouse model of experimental sepsis. We show that decreased plasma kallikrein concentration in septic mice is a result of reduced mRNA expression plasma prekallikrein gene, indicating that plasma kallikrein belong to negative acute phase proteins. Investigations regarding the pathophysiological function of contact system proteases during sepsis revealed different roles for factor XII and plasma kallikrein.
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Registered trials
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