ArticleThe American journal of pathology2002
Shock-induced neutrophil mediated priming for acute lung injury in mice: divergent effects of TLR-4 and TLR-4/FasL deficiency.
Article in The American journal of pathology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.
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Who cites it
73 citing papers in PubMed, 149 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
- V-domain Ig Suppressor of T cell Activation Expression During Hemorrhage or Sepsis-Induced Acute Respiratory Distress Syndrome: Insights From a Mouse Model.The Journal of surgical research · 2025Article
- VISTA functions as a protective immune checkpoint in indirect acute respiratory distress syndrome by modulating systemic and compartmentalized inflammation.Frontiers in immunology · 2025Article
- Application of single cell multiomics points to changes in chromatin accessibility near calcitonin receptor like receptor and a possible role for adrenomedullin in the post-shock lung.Frontiers in medicine · 2023Article
- Lymphocyte HVEM/BTLA co-expression after critical illness demonstrates severity indiscriminate upregulation, impacting critical illness-induced immunosuppression.Frontiers in medicine · 2023Article
- The Actin-Binding Protein Cortactin Promotes Sepsis Severity by Supporting Excessive Neutrophil Infiltration into the Lung.Biomedicines · 2022Article
- The journey of SARS-CoV-2 in human hosts: a review of immune responses, immunosuppression, and their consequences.Virulence · 2021Review
- Murine Myeloid Progenitors Attenuate Immune Dysfunction Induced by Hemorrhagic Shock.Stem cell reports · 2021Article
- Survival and Pulmonary Injury After Neonatal Sepsis: PD1/PDL1's Contributions to Mouse and Human Immunopathology.Frontiers in immunology · 2021Article
- SHP2 inhibitor PHPS1 ameliorates acute kidney injury by Erk1/2-STAT3 signaling in a combined murine hemorrhage followed by septic challenge model.Molecular medicine (Cambridge, Mass.) · 2020Article
- Alternative RNA splicing and alternative transcription start/end in acute respiratory distress syndrome.Intensive care medicine · 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
- RNAi therapeutic strategies for acute respiratory distress syndrome.Translational research : the journal of laboratory and clinical medicine · 2019Review
- Hemorrhage Attenuates Neutrophil Recruitment in Response to Secondary Respiratory Infection by Pseudomonas Aeruginosa.Shock (Augusta, Ga.) · 2019Article
- Does Neutrophil Phenotype Predict the Survival of Trauma Patients?Frontiers in immunology · 2019Review
- Changes in the process of alternative RNA splicing results in soluble B and T lymphocyte attenuator with biological and clinical implications in critical illness.Molecular medicine (Cambridge, Mass.) · 2018Article
- PAD4 Deficiency Leads to Decreased Organ Dysfunction and Improved Survival in a Dual Insult Model of Hemorrhagic Shock and Sepsis.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- A novel role for coinhibitory receptors/checkpoint proteins in the immunopathology of sepsis.Journal of leukocyte biology · 2018Review
13 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Acute lung injury (ALI) leading to respiratory distress is a common sequela of shock/trauma, however, modeling this process in mice with a single shock or septic event is inconsistent. One explanation is that hemorrhage is often just a "priming insult," thus, secondary stimuli may be required to "trigger" ALI. To test this we carried out studies in which we assessed the capacity of hemorrhage alone or hemorrhage followed by septic challenge (CLP) to induce ALI. Lung edema, bronchoalveolar lavage interleukin (IL)-6, alveolar congestion, as well as lung IL-6, macrophage inflammatory protein (MIP)-2, and myeloperoxidase (MPO) activity were all increased in mice subjected to CLP at 24 but not 72 hours following hemorrhage. This was associated with a marked increase in the susceptibility of these mice to septic mortality. Peripheral blood neutrophils derived from 24 hours post-hemorrhage, but not Sham animals, exhibited an ex vivo decrease in apoptotic frequency and an increase in respiratory burst capacity, consistent with in vivo "priming." Subsequently, we observed that adoptive transfer of neutrophils from hemorrhaged but not sham-hemorrhage animals to neutropenic recipients reproduce ALI when subsequently septically challenged, implying that this priming was mediated by neutrophils. We also found marked general increases in lung IL-6, MIP-2, and MPO in mice deficient for toll-like receptor (TLR-4) or the combined lack of TLR-4/FasL. However, the TLR-4 defect markedly attenuated neutrophil influx into the lung while not altering the change in local cytokine/chemokine expression. Alternatively, the combined loss of FasL and TLR-4 did not inhibit the increase in MPO and exacerbated lung IL-6/MIP-2 levels even further.
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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.