ArticleScientific reports2016
Myeloid tissue factor does not modulate lung inflammation or permeability during experimental acute lung injury.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- Matrix metalloproteinase-7 is dispensable in a mouse model of sepsis-induced acute lung injury.PloS one · 2025Article
- Cell-free hemoglobin triggers macrophage cytokine production via TLR4 and MyD88.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- Liraglutide pretreatment attenuates sepsis-induced acute lung injury.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- A two-hit model of sepsis plus hyperoxia causes lung permeability and inflammation.American journal of physiology. Lung cellular and molecular physiology · 2022Article
- Antioxidants as Therapeutic Agents in Acute Respiratory Distress Syndrome (ARDS) Treatment-From Mice to Men.Biomedicines · 2022Review
- An aberrant STAT pathway is central to COVID-19.Cell death and differentiation · 2020Review
- The NLRP3 inflammasome in macrophages is stimulated by cell-free hemoglobin.Physiological reports · 2020Article
- The coagulation system in host defense.Research and practice in thrombosis and haemostasis · 2018Review
- GBT1118, a compound that increases the oxygen affinity of hemoglobin, improves survival in murine hypoxic acute lung injury.Journal of applied physiology (Bethesda, Md. : 1985) · 2018Article
- ICAM-1-targeted thrombomodulin mitigates tissue factor-driven inflammatory thrombosis in a human endothelialized microfluidic model.Blood advances · 2017Article
- Myeloid but not epithelial tissue factor exerts protective anti-inflammatory effects in acid aspiration-induced acute lung injury.Journal of thrombosis and haemostasis : JTH · 2017Article
- Chemomics-Integrated Proteomics Analysis of Jie-Geng-Tang to Ameliorate Lipopolysaccharide-Induced Acute Lung Injury in Mice.Evidence-based complementary and alternative medicine : eCAM · 2016Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Tissue factor (TF) is a critical mediator of direct acute lung injury (ALI) with global TF deficiency resulting in increased airspace inflammation, alveolar-capillary permeability, and alveolar hemorrhage after intra-tracheal lipopolysaccharide (LPS). In the lung, TF is expressed diffusely on the lung epithelium and intensely on cells of the myeloid lineage. We recently reported that TF on the lung epithelium, but not on myeloid cells, was the major source of TF during intra-tracheal LPS-induced ALI. Because of a growing body of literature demonstrating important pathophysiologic differences between ALI caused by different etiologies, we hypothesized that TF on myeloid cells may have distinct contributions to airspace inflammation and permeability between direct and indirect causes of ALI. To test this, we compared mice lacking TF on myeloid cells (TF(∆mye), LysM.Cre(+/-)TF(flox/flox)) to littermate controls during direct (bacterial pneumonia, ventilator-induced ALI, bleomycin-induced ALI) and indirect ALI (systemic LPS, cecal ligation and puncture). ALI was quantified by weight loss, bronchoalveolar lavage (BAL) inflammatory cell number, cytokine concentration, protein concentration, and BAL procoagulant activity. There was no significant contribution of TF on myeloid cells in multiple models of experimental ALI, leading to the conclusion that TF in myeloid cells is not a major contributor to experimental ALI.
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Registered trials
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