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Circulating mitochondrial DAMPs cause inflammatory responses to injury

Nature, 2010-03, Vol.464 (7285), p.104-107

2010

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Mitochondrial DNA is released by shock and activates neutrophils via p38 map kinase

Shock (Augusta, Ga.), 2010-07, Vol.34 (1), p.55-59

2010

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Scavenging Circulating Mitochondrial DNA as a Potential Therapeutic Option for Multiple Organ Dysfunction in Trauma Hemorrhage

Frontiers in immunology, 2018-05, Vol.9, p.891-891

2018

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Plasma bacterial and mitochondrial DNA distinguish bacterial sepsis from sterile systemic inflammatory response syndrome and quantify inflammatory tissue injury in nonhuman primates

Shock (Augusta, Ga.), 2013-01, Vol.39 (1), p.55-62

2013

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Mitochondrial Damage Associated Molecular Patterns From Femoral Reamings Activate Neutrophils Through Formyl Peptide Receptors and P44/42 MAP Kinase

Journal of orthopaedic trauma, 2010-09, Vol.24 (9), p.534-538

2010

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Heme as a danger molecule in pathogen recognition

Free radical biology & medicine, 2015-12, Vol.89, p.651-661

2015

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Trauma-induced heme release increases susceptibility to bacterial infection

JCI insight, 2021-10, Vol.6 (20)

2021

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Role of Mitochondria-Derived Danger Signals Released After Injury in Systemic Inflammation and Sepsis

Antioxidants & redox signaling, 2021-11, Vol.35 (15), p.1273

2021

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Neutrophil activation is modulated by sex hormones after trauma-hemorrhagic shock and burn injuries

American journal of physiology. Heart and circulatory physiology, 2006-09, Vol.291 (3), p.H1456-H1465

2006

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Extracellular mitochondria drive CD8 T cell dysfunction in trauma by upregulating CD39

Thorax, 2023-02, Vol.78 (2), p.151-159

2023

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Plasma and wound fluids from trauma patients suppress neutrophil extracellular respiratory burst

The journal of trauma and acute care surgery, 2022-02, Vol.92 (2), p.330-338

2022

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Cytomegalovirus durably primes neutrophil oxidative burst

Journal of leukocyte biology, 2023-10, Vol.114 (5), p.459-474

2023

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Formyl Peptide Receptor-1 Blockade Prevents Receptor Regulation by Mitochondrial Danger-Associated Molecular Patterns and Preserves Neutrophil Function After Trauma

Critical care medicine, 2020-02, Vol.48 (2), p.e123

2020

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Mitochondrial damage-associated molecular patterns released by abdominal trauma suppress pulmonary immune responses

The journal of trauma and acute care surgery, 2014-05, Vol.76 (5), p.1222-1227

2014

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Intratracheal instillation of neutrophils rescues bacterial overgrowth initiated by trauma damage-associated molecular patterns

The journal of trauma and acute care surgery, 2017-05, Vol.82 (5), p.853-860

2017

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Direct Airway Instillation of Neutrophils Overcomes Chemotactic Deficits Induced by Injury

Shock (Augusta, Ga.), 2021-07, Vol.56 (1), p.119-124

2021

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An Integrated Pharmacological, Structural, and Genetic Analysis of Extracellular Versus Intracellular ROS Production in Neutrophils

Journal of molecular biology, 2022-05, Vol.434 (9), p.167533-167533, Article 167533

2022

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Preclinical models of traumatic, hemorrhagic shock

Shock (Augusta, Ga.), 2005-12, Vol.24 Suppl 1 (Supplement 1), p.24-32

Hauser, Carl J

2005

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Mitochondrial damage-associated molecular patterns from fractures suppress pulmonary immune responses via formyl peptide receptors 1 and 2

The journal of trauma and acute care surgery, 2015-02, Vol.78 (2), p.272-281

2015

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A “CLEAN CASE” OF SYSTEMIC INJURY: MESENTERIC LYMPH AFTER HEMORRHAGIC SHOCK ELICITS A STERILE INFLAMMATORY RESPONSE

Shock (Augusta, Ga.), 2015-10, Vol.44 (4), p.336-340

2015

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NADPH oxidase and Nrf2 regulate gastric aspiration-induced inflammation and acute lung injury

The Journal of immunology (1950), 2013-02, Vol.190 (4), p.1714-1724

2013

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Trauma-hemorrhage-induced neutrophil priming is prevented by mesenteric lymph duct ligation

Shock (Augusta, Ga.), 2002-12, Vol.18 (6), p.513-517

2002

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Na+/H+ exchanger blockade inhibits enterocyte inflammatory response and protects against colitis

American journal of physiology: Gastrointestinal and liver physiology, 2002-07, Vol.283 (1), p.G122-G132

2002

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Challenges to effective research in acute trauma resuscitation: consent and endpoints

Shock (Augusta, Ga.), 2011-02, Vol.35 (2), p.107-113

2011

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Hypertonic saline resuscitation limits neutrophil activation after trauma-hemorrhagic shock

Shock (Augusta, Ga.), 2003-04, Vol.19 (4), p.328-333

2003

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Circulating mitochondrial DAMPs cause inflammatory responses to injury

Mitochondrial DNA is released by shock and activates neutrophils via p38 map kinase

Scavenging Circulating Mitochondrial DNA as a Potential Therapeutic Option for Multiple Organ Dysfunction in Trauma Hemorrhage

Plasma bacterial and mitochondrial DNA distinguish bacterial sepsis from sterile systemic inflammatory response syndrome and quantify inflammatory tissue injury in nonhuman primates

Mitochondrial Damage Associated Molecular Patterns From Femoral Reamings Activate Neutrophils Through Formyl Peptide Receptors and P44/42 MAP Kinase

Heme as a danger molecule in pathogen recognition

Trauma-induced heme release increases susceptibility to bacterial infection

Role of Mitochondria-Derived Danger Signals Released After Injury in Systemic Inflammation and Sepsis

Neutrophil activation is modulated by sex hormones after trauma-hemorrhagic shock and burn injuries

Extracellular mitochondria drive CD8 T cell dysfunction in trauma by upregulating CD39

Plasma and wound fluids from trauma patients suppress neutrophil extracellular respiratory burst

Cytomegalovirus durably primes neutrophil oxidative burst

Formyl Peptide Receptor-1 Blockade Prevents Receptor Regulation by Mitochondrial Danger-Associated Molecular Patterns and Preserves Neutrophil Function After Trauma

Mitochondrial damage-associated molecular patterns released by abdominal trauma suppress pulmonary immune responses

Intratracheal instillation of neutrophils rescues bacterial overgrowth initiated by trauma damage-associated molecular patterns

Direct Airway Instillation of Neutrophils Overcomes Chemotactic Deficits Induced by Injury

An Integrated Pharmacological, Structural, and Genetic Analysis of Extracellular Versus Intracellular ROS Production in Neutrophils

Preclinical models of traumatic, hemorrhagic shock

Mitochondrial damage-associated molecular patterns from fractures suppress pulmonary immune responses via formyl peptide receptors 1 and 2

A “CLEAN CASE” OF SYSTEMIC INJURY: MESENTERIC LYMPH AFTER HEMORRHAGIC SHOCK ELICITS A STERILE INFLAMMATORY RESPONSE

NADPH oxidase and Nrf2 regulate gastric aspiration-induced inflammation and acute lung injury

Trauma-hemorrhage-induced neutrophil priming is prevented by mesenteric lymph duct ligation

Na+/H+ exchanger blockade inhibits enterocyte inflammatory response and protects against colitis

Challenges to effective research in acute trauma resuscitation: consent and endpoints

Hypertonic saline resuscitation limits neutrophil activation after trauma-hemorrhagic shock

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