Tobias A. Fuchs

ORCID: 0000-0001-6690-6962
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About
Contact & Profiles
Research Areas
  • Neutrophil, Myeloperoxidase and Oxidative Mechanisms
  • Blood disorders and treatments
  • Coagulation, Bradykinin, Polyphosphates, and Angioedema
  • Blood Coagulation and Thrombosis Mechanisms
  • Cell Adhesion Molecules Research
  • Immune cells in cancer
  • Venous Thromboembolism Diagnosis and Management
  • Vasculitis and related conditions
  • Protease and Inhibitor Mechanisms
  • Complement system in diseases
  • Mast cells and histamine
  • Urticaria and Related Conditions
  • Nitric Oxide and Endothelin Effects
  • Immune Response and Inflammation
  • Platelet Disorders and Treatments
  • Intestinal and Peritoneal Adhesions
  • Acute Myeloid Leukemia Research
  • Inflammasome and immune disorders
  • Eosinophilic Disorders and Syndromes
  • Mechanical Circulatory Support Devices
  • Neonatal and Maternal Infections
  • Testicular diseases and treatments
  • Hemoglobinopathies and Related Disorders
  • Intraperitoneal and Appendiceal Malignancies
  • Sepsis Diagnosis and Treatment

University Medical Center Hamburg-Eppendorf
2015-2025

Universität Hamburg
2015-2025

Innsbruck Medical University
2024

Universität Innsbruck
2024

Heidelberg University
2023

University Hospital Heidelberg
2023

University Medical Centre Mannheim
2023

Karolinska Institutet
2014-2018

Karolinska University Hospital
2014-2017

Boston Children's Hospital
2009-2015

Neutrophil extracellular traps (NETs) are structures composed of chromatin and granule proteins that bind kill microorganisms. We show upon stimulation, the nuclei neutrophils lose their shape, eu- heterochromatin homogenize. Later, nuclear envelope membranes disintegrate, allowing mixing NET components. Finally, NETs released as cell membrane breaks. This death process is distinct from apoptosis necrosis depends on generation reactive oxygen species (ROS) by NADPH oxidase. Patients with...

10.1083/jcb.200606027 article EN The Journal of Cell Biology 2007-01-08

Neutrophil extracellular traps (NETs) are part of the innate immune response to infections. NETs a meshwork DNA fibers comprising histones and antimicrobial proteins. Microbes immobilized in encounter locally high lethal concentration effector Recent studies show that formed inside vasculature infections noninfectious diseases. Here we report provide heretofore unrecognized scaffold stimulus for thrombus formation. perfused with blood caused platelet adhesion, activation, aggregation. DNase...

10.1073/pnas.1005743107 article EN Proceedings of the National Academy of Sciences 2010-08-23

Cancer-associated thrombosis often lacks a clear etiology. However, it is linked to poor prognosis and represents the second-leading cause of death in cancer patients. Recent studies have shown that chromatin released into blood, through generation neutrophil extracellular traps (NETs), procoagulant prothrombotic. Using murine model chronic myelogenous leukemia, we show malignant nonmalignant neutrophils are more prone NET formation. This increased sensitivity toward also observed mammary...

10.1073/pnas.1200419109 article EN Proceedings of the National Academy of Sciences 2012-07-23

Blood DNases hack the NET Neutrophil extracellular traps (NETs) are lattices of processed chromatin decorated with select secreted and cytoplasmic proteins that trap neutralize microbes. However, their inappropriate release may do more harm than good by promoting inflammation thrombosis. Jiménez-Alcázar et al. report two deoxyribonucleases (DNases), DNASE1 DNASE1L3, have partially redundant roles in degrading NETs circulation (see Perspective Gunzer). Knockout mice lacking these enzymes were...

10.1126/science.aam8897 article EN Science 2017-11-30

Deep vein thrombosis and pulmonary embolism are major health problems associated with high mortality. Recently, DNA-based neutrophil extracellular traps (NETs) resulting from the release of decondensed chromatin, were found to be part thrombus scaffold promote coagulation. However, significance nuclear decondensation NET generation in is largely unknown. To address this, we adopted a stenosis model deep analyzed venous thrombi peptidylarginine deiminase 4 (PAD4)-deficient mice that cannot...

10.1073/pnas.1301059110 article EN Proceedings of the National Academy of Sciences 2013-05-06

Objective— Aberrant neutrophil activation occurs during the advanced stages of atherosclerosis. Once primed, neutrophils can undergo apoptosis or release extracellular traps. This DNA exerts potent proinflammatory, prothrombotic, and cytotoxic properties. The goal this study was to examine relationships among formation, coronary atherosclerosis, presence a prothrombotic state. Approach Results— In prospective, observational, cross-sectional cohort 282 individuals with suspected artery...

10.1161/atvbaha.113.301627 article EN Arteriosclerosis Thrombosis and Vascular Biology 2013-07-02

Human and murine platelets (PLTs) variably express toll-like receptors (TLRs), which link the innate adaptive immune responses during infectious inflammation atherosclerotic vascular disease. In this paper, we show that TLR9 transcript is specifically up-regulated pro-PLT production distributed to a novel electron-dense tubular system-related compartment have named T granule. colocalizes with protein disulfide isomerase associated either VAMP 7 or 8, regulates its distribution in PLTs on...

10.1083/jcb.201111136 article EN cc-by-nc-sa The Journal of Cell Biology 2012-08-20

Objective— Recently, a growing number of studies have revealed prothrombotic and cytotoxic role for extracellular chromatin. Cerebral ischemia/reperfusion injury is characterized by significant amount cell death neutrophil activation, both which may result in the release The goal this study was to assess effect chromatin ischemic stroke using mouse model transient middle cerebral artery occlusion. Methods Results— Similar reports patients, we observed increased levels circulating nucleosomes...

10.1161/atvbaha.112.250993 article EN Arteriosclerosis Thrombosis and Vascular Biology 2012-05-25
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