ArticleShock (Augusta, Ga.)2012
The role and source of tumor necrosis factor-α in hemorrhage-induced priming for septic lung injury.
Article in Shock (Augusta, Ga.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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.
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Who cites it
28 citing papers in PubMed, 42 citations in OpenAlex.
- Endothelial cell, but not neutrophil, programmed cell death receptor-ligand 1 loss has a morbid impact on experimental murine shock/sepsis-induced lung injury.Frontiers in immunology · 2026Article
- Differential Effects of Endothelial Cell- as opposed to Neutrophil-Lineage Restricted PD-L1 Gene Expression on Experimental Murine Shock/ Sepsis-Induced Lung Injury.Research square · 2025Article
- Mechanisms of immune suppression in sepsis/shock: one investigator's/lab group's experience (SLB 2024 legacy award presentation).Journal of leukocyte biology · 2025Article
- Role of mesenchymal stem cells in sepsis and their therapeutic potential in sepsis‑associated myopathy (Review).International journal of molecular medicine · 2024Review
- 17β-Estradiol Abrogates TNF-α-Induced Human Brain Vascular Pericyte Migration by Downregulating miR-638 via ER-β.International journal of molecular sciences · 2024Article
- Chronic Heat Stress Induces Oxidative Stress and Induces Inflammatory Injury in Broiler Spleen via TLRs/MyD88/NF-κB Signaling Pathway in Broilers.Veterinary sciences · 2024Article
- miRNA-206-3p alleviates LPS-induced acute lung injury via inhibiting inflammation and pyroptosis through modulating TLR4/NF-κB/NLRP3 pathway.Scientific reports · 2024Article
- Effect of saffron, black seed, and their main constituents on inflammatory cytokine response (mainly TNF-α) and oxidative stress status: an aspect on pharmacological insights.Naunyn-Schmiedeberg's archives of pharmacology · 2023Review
- Progress in non-viral localized delivery of siRNA therapeutics for pulmonary diseases.Acta pharmaceutica Sinica. B · 2023Review
- Left ventricular assist devices promote changes in the expression levels of platelet microRNAs.Frontiers in cardiovascular medicine · 2023Article
- MKK4 Knockdown Plays a Protective Role in Hemorrhagic Shock-Induced Liver Injury through the JNK Pathway.Oxidative medicine and cellular longevity · 2022Article
- The role and mechanism of the annexin A1 peptide Ac2-26 in rats with cardiopulmonary bypass lung injury.Basic & clinical pharmacology & toxicology · 2021Article
- Murine Myeloid Progenitors Attenuate Immune Dysfunction Induced by Hemorrhagic Shock.Stem cell reports · 2021Article
- Deoxyribonuclease Reduces Tissue Injury and Improves Survival After Hemorrhagic Shock.The Journal of surgical research · 2020Article
- Blockade of endothelial, but not epithelial, cell expression of PD-L1 following severe shock attenuates the development of indirect acute lung injury in mice.American journal of physiology. Lung cellular and molecular physiology · 2020Article
- Alpha-1-Antitrypsin Ameliorates Pristane Induced Diffuse Alveolar Hemorrhage in Mice.Journal of clinical medicine · 2019Article
- Anti-interferon-α receptor 1 antibodies attenuate inflammation and organ injury following hemorrhagic shock.The journal of trauma and acute care surgery · 2019Article
- Herpes Virus Entry Mediator (HVEM) Expression Promotes Inflammation/ Organ Injury in Response to Experimental Indirect-Acute Lung Injury.Shock (Augusta, Ga.) · 2019Article
- A novel role for coinhibitory receptors/checkpoint proteins in the immunopathology of sepsis.Journal of leukocyte biology · 2018Review
- Messenger RNA sequencing reveals similar mechanisms between neonatal and acute respiratory distress syndrome.Molecular medicine reports · 2018Article
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 3 countries.
Funding
Abstract
Tumor necrosis factor α (TNF-α) has been reported to be a key component of the functional priming, of both myeloid and nonmyeloid cells, that is thought to contribute to the lung's increased susceptibility to injury following shock. Not surprisingly, we found that mice deficient in TNF-α exhibited reduced acute lung injury (ALI) resultant from the combined insults of hemorrhagic shock and sepsis. However, we found that when we adoptively transferred neutrophils from mice expressing TNF-α to neutrophil-depleted mice that lacked TNF-α, they were not able to serve as priming stimulus for the development of ALI. Based on these findings, we proposed that resident lung tissue cells mediate TNF-α priming. To begin to unravel the complex signaling pathway of various resident lung tissue cells in TNF-α-induced priming, we compared the effect of local (intratracheal [i.t.]) versus systemic [intravenous (i.v.)] delivery of TNF-α small interference (siRNA). We hypothesized that alternately suppressing expression of TNF-α in lung endothelial (i.v.) or epithelial (i.t.) cells would produce a differential effect in shock-induced ALI. We found that when in vivo siRNA i.t. or i.v. against TNF-α was administered to C57/BL6 mice at 2 h after hemorrhage, 24 h before septic challenge, that systemic/i.v., but not i.t., delivery of TNF-α siRNA following hemorrhage priming significantly reduces expression of indices of ALI compared with controls. These findings suggest that an absence of local lung tissue TNF-α significantly reduces lung tissue injury following hemorrhage priming for ALI and that pulmonary endothelial and/or other possible vascular resident cells, not epithelial cells, play a greater role in mediating the TNF-α priming response in a mouse model of hemorrhage/sepsis-induced ALI.
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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.