ArticleExperimental and molecular pathology2012
Fingerprinting of the TLR4-induced acute inflammatory response.
Article in Experimental and molecular pathology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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.
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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
18 citing papers in PubMed.
- Proton-activated chloride channel 1 is essential for innate host defense against bacterial sepsis.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Protective Effect of Low 2-O, 3-O Desulfated Heparin (ODSH) Against LPS-Induced Acute Lung Injury in Mice.Biomolecules · 2025Article
- Myeloid cell-derived interleukin-6 induces vascular dysfunction and vascular and systemic inflammation.European heart journal open · 2024Article
- Dynamic RBM47 ISGylation confers broad immunoprotection against lung injury and tumorigenesis via TSC22D3 downregulation.Cell death discovery · 2023Article
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- The pituitary gland prevents shock-associated death by controlling multiple inflammatory mediators.Biochemical and biophysical research communications · 2019Article
- Penehyclidine hydrochloride inhibits TLR4 signaling and inflammation, and attenuates blunt chest trauma and hemorrhagic shock-induced acute lung injury in rats.Molecular medicine reports · 2018Article
- Effect of anti-podoplanin antibody administration during lipopolysaccharide-induced lung injury in mice.BMJ open respiratory research · 2017Article
- Role of NOD2 and RIP2 in host-microbe interactions with Gram-negative bacteria: insights from the periodontal disease model.Innate immunity · 2016Article
- Effects of atorvastatin combined with low-molecular-weight heparin on plasma inflammatory cytokine level and pulmonary pathophysiology of rats with sepsis.Experimental and therapeutic medicine · 2016Article
- Enhanced resolution of experimental ARDS through IL-4-mediated lung macrophage reprogramming.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- Endotoxemia-mediated inflammation potentiates aminoglycoside-induced ototoxicity.Science translational medicine · 2015Article
- CRF-amplified neuronal TLR4/MCP-1 signaling regulates alcohol self-administration.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2015Article
- Systemic lipopolysaccharide induces cochlear inflammation and exacerbates the synergistic ototoxicity of kanamycin and furosemide.Journal of the Association for Research in Otolaryngology : JARO · 2014Article
- LPS response pattern of inflammatory adipokines in an in vitro 3T3-L1 murine adipocyte model.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2014Article
- Inhibition of the phosphoinositide 3-kinase pathway decreases innate resistance to lipopolysaccharide toxicity in TLR4 deficient mice.Journal of biomedical science · 2014Article
- CD11c+ alveolar macrophages are a source of IL-23 during lipopolysaccharide-induced acute lung injury.Shock (Augusta, Ga.) · 2013Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Intensive scientific efforts in the past decades have helped shed light into the pathogenesis of endotoxin-induced inflammation. We have used multiplexing bead-based assays to characterize the responses in two models of in vivo LPS challenge. C57BL/6 mice were either injected intraperitoneally (endotoxemia) or intratracheally (acute lung injury; ALI) with lipopolysaccharide (LPS). The time courses (1h-24h) of the following 20 inflammatory mediators in plasma or broncho-alveolar lavages were simultaneously analyzed: IL-1α, IL-1β, IL-2, IL-3, IL-4, IL-5, IL-6, IL-9, IL-12(p40), IL-13, Eotaxin (CCL11), G-CSF, GM-CSF, IFN-γ, KC (CXCL1), MCP-1 (CCL2), MIP-1α (CCL3), MIP-1β (CCL4), RANTES (CCL5) and TNF-α. While significant inductions of all mediators were found, substantial differences in their absolute concentrations, time points of maximal concentrations and clearances were observed. There were also notable variations in the patterns of several cytokines/chemokines when samples from endotoxemia and LPS-ALI were compared. These data may be helpful in defining analytic strategies including selection of optimal time points for studying the host immune response to endotoxin.
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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.