ArticleInfection and immunity2012
Factor XI-deficient mice display reduced inflammation, coagulopathy, and bacterial growth during listeriosis.
Article in Infection and immunity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
25 citing papers in PubMed, 34 citations in OpenAlex.
- Contact Activation Inhibitor and Factor XI Antibody, AB023, Produces Safe, Dose-Dependent Anticoagulation in a Phase 1 First-In-Human Trial.Arteriosclerosis, thrombosis, and vascular biology · 2019Trial
- The Interaction of Complement and Intrinsic Coagulation System: A Comparative Study between COVID-19 and Bacterial Sepsis Patients.Journal of clinical medicine · 2024Article
- Review
- Activation of coagulation FXI promotes endothelial inflammation and amplifies platelet activation in a nonhuman primate model of hyperlipidemia.Research and practice in thrombosis and haemostasis · 2024Article
- First case of aorto-bi-iliac endograft thrombotic infection byExperimental and therapeutic medicine · 2022Article
- Association of FXI activity with thrombo-inflammation, extracellular matrix, lipid metabolism and apoptosis in venous thrombosis.Scientific reports · 2022Article
- Article
- Cross-Talk between the Complement Pathway and the Contact Activation System of Coagulation: Activated Factor XI Neutralizes Complement Factor H.Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- The rebirth of the contact pathway: a new therapeutic target.Current opinion in hematology · 2020Review
- Pharmacological Agents Targeting Thromboinflammation in COVID-19: Review and Implications for Future Research.Thrombosis and haemostasis · 2020Review
- The contact activation system as a potential therapeutic target in patients with COVID-19.Research and practice in thrombosis and haemostasis · 2020Article
- A non-circulating pool of factor XI associated with glycosaminoglycans in mice.Journal of thrombosis and haemostasis : JTH · 2019Article
- The contact pathway and sepsis.Research and practice in thrombosis and haemostasis · 2019Review
- Inhibition of contact-mediated activation of factor XI protects baboons againstBlood advances · 2019Article
- Plasma contact factors as therapeutic targets.Blood reviews · 2018Review
- Recent advances in the discovery and development of factor XI/XIa inhibitors.Medicinal research reviews · 2018Review
- Factor XI and pulmonary infections.Haemophilia : the official journal of the World Federation of Hemophilia · 2018Article
- Article
- Factor XI Deficiency Protects Against Atherogenesis in Apolipoprotein E/Factor XI Double Knockout Mice.Arteriosclerosis, thrombosis, and vascular biology · 2016Article
- Factor XIa inhibitors: A review of the patent literature.Expert opinion on therapeutic patents · 2016Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
In mice infected sublethally with Listeria monocytogenes, fibrin is deposited at low levels within hepatic tissue, where it functions protectively by limiting bacterial growth and suppressing hemorrhagic pathology. Here we demonstrate that mice infected with lethal doses of L. monocytogenes produce higher levels of fibrin and display evidence of systemic coagulopathy (i.e., thrombocytopenia, fibrinogen depletion, and elevated levels of thrombin-antithrombin complexes). When the hepatic bacterial burden exceeds 1×10(6) CFU, levels of hepatic fibrin correlate with the bacterial burden, which also correlates with levels of hepatic mRNA encoding the hemostatic enzyme factor XI (FXI). Gene-targeted FXI-deficient mice show significantly improved survival upon challenge with high doses of L. monocytogenes and also display reduced levels of hepatic fibrin, decreased evidence of coagulopathy, and diminished cytokine production (interleukin-6 [IL-6] and IL-10). While fibrin limits the bacterial burden during sublethal listeriosis in wild-type mice, FXI-deficient mice display a significantly improved capacity to restrain the bacterial burden during lethal listeriosis despite their reduced fibrin levels. They also show less evidence of hepatic necrosis. In conjunction with suboptimal antibiotic therapy, FXI-specific monoclonal antibody 14E11 improves survival when administered therapeutically to wild-type mice challenged with high doses of L. monocytogenes. Together, these findings demonstrate the utility of murine listeriosis as a model for dissecting qualitative differences between protective and pathological host responses and reveal novel roles for FXI in exacerbating inflammation and pathogen burden during a lethal bacterial infection.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.