ArticleThe American journal of pathology2012
LPS-induced murine systemic inflammation is driven by parenchymal cell activation and exclusively predicted by early MCP-1 plasma levels.
Article in The American journal of pathology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
What it found
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Who cites it
37 citing papers in PubMed.
- Trial
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- Transcranial photoacoustic imaging of indocyanine green J-aggregates reveals cerebral signal changes in lipopolysaccharide-induced systemic inflammation.Photoacoustics · 2026Article
- Targeting T cell metabolism and polarization to modulate post-stroke immune responses and improve outcomes.Frontiers in immunology · 2026Article
- Article
- Enhancing natural killer cell anti-tumour activity through macrophage manipulation.Frontiers in immunology · 2025Review
- Microglia drive diurnal variation in susceptibility to inflammatory blood-brain barrier breakdown.JCI insight · 2024Article
- Article
- 4R-cembranoid suppresses glial cells inflammatory phenotypes and prevents hippocampal neuronal loss in LPS-treated mice.Journal of neuroscience research · 2024Article
- Effect of mitoTEMPO on Redox Reactions in Different Body Compartments upon Endotoxemia in Rats.Biomolecules · 2023Article
- Water Extract ofNutrients · 2023Article
- Vitronectin promotes immunothrombotic dysregulation in the venular microvasculature.Frontiers in immunology · 2023Article
- The complex lipid, SPPCT-800, reduces lung damage, improves pulmonary function and decreases pro-inflammatory cytokines in the murine LPS-induced acute respiratory distress syndrome (ARDS) model.Pharmaceutical biology · 2022Article
- Absence of CCR2 Promotes Proliferation of Alveolar Macrophages That Control Lung Inflammation in Acute Respiratory Distress Syndrome in Mice.International journal of molecular sciences · 2022Article
- Hydro-ethanol extract of Holarrhena floribunda stem bark exhibits anti-anaphylactic and anti-oedematogenic effects in murine models of acute inflammation.BMC complementary medicine and therapies · 2022Article
- Acute Inflammation Confers Enhanced Protection against Mycobacterium tuberculosis Infection in Mice.Microbiology spectrum · 2021Article
- Modular complement assemblies for mitigating inflammatory conditions.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Chronic Kidney Disease Increases Cerebral Microbleeds in Mouse and Man.Translational stroke research · 2020Article
- Photosynthesis-inspired HNature communications · 2020Article
- The Receptor for Advanced Glycation Endproducts (RAGE) Contributes to Severe Inflammatory Liver Injury in Mice.Frontiers in immunology · 2020Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Systemic inflammation remains a major cause of morbidity and mortality in the United States, across many disease processes. One classic murine model to study this syndrome is lipopolysaccharide (LPS)-induced Toll-like receptor 4 (TLR4)-dependent systemic inflammation. Although most studies have focused on inflammatory cell TLR4 responses, parenchymal cells also express TLR4. Our objective was to define the in vivo role of parenchymal- versus marrow-derived cell activation via TLR4 during LPS-induced inflammation. Mice bearing TLR4 on parenchymal cells only, marrow-derived cells only, both, or neither were generated using bone marrow transplantation. Mortality occurred only in mice that had TLR4 expression on their parenchymal cells. Before onset, virtually all major plasma cytokines and blood neutrophil responses were related to marrow-derived cell activation via TLR4. The only cytokine predictive of oncoming systemic inflammation was the chemokine monocyte chemoattractant protein-1. Late blood neutrophil responses were related to the presence of TLR4 on either parenchymal or marrow cells, whereas plasma cytokine elevations late in LPS-induced systemic inflammation were dependent on mice having TLR4 in both cell compartments. Parenchymal cell activation via TLR4 is a key component of LPS-induced systemic inflammation and mortality, although most plasma cytokine levels and blood neutrophil responses were not key components. Given its unique role, future studies into monocyte chemoattractant protein-1's exact role during systemic inflammation are warranted.
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