ArticleThe Journal of clinical investigation1996
Role of the intercellular adhesion molecule-1(ICAM-1) in endotoxin-induced pneumonia evaluated using ICAM-1 antisense oligonucleotides, anti-ICAM-1 monoclonal antibodies, and ICAM-1 mutant mice.
Article in The Journal of clinical investigation, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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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
42 citing papers in PubMed, 201 citations in OpenAlex.
- Trial
- Nanoparticle-based approaches for vascular inflammation in managing hypertension: advancing molecular mechanisms and treatment strategies.Drug delivery and translational research · 2026Review
- Mechanism of arterial injury exacerbated by hyperhomocysteinemia in spontaneously hypertensive rats.Scientific reports · 2023Article
- E3 Ubiquitin Ligase Midline 1 Regulates Endothelial Cell ICAM-1 Expression and Neutrophil Adhesion in Abdominal Sepsis.International journal of molecular sciences · 2022Article
- Targeting vascular inflammation through emerging methods and drug carriers.Advanced drug delivery reviews · 2022Review
- ICAM-1 and ICAM-2 Are Differentially Expressed and Up-Regulated on Inflamed Pulmonary Epithelium, but Neither ICAM-2 nor LFA-1: ICAM-1 Are Required for Neutrophil Migration Into the AirwaysFrontiers in immunology · 2021Article
- HGF Reduces Disease Severity and Inflammation by Attenuating the NF-κB Signaling in a Rat Model of Pulmonary Artery Hypertension.Inflammation · 2018Article
- Predicted effects of observed changes in the mRNA and microRNA transcriptome of lung neutrophils during S. pneumoniae pneumonia in mice.Scientific reports · 2017Article
- A Critical Role for P2X7 Receptor-Induced VCAM-1 Shedding and Neutrophil Infiltration during Acute Lung Injury.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Inducible RasGEF1B circular RNA is a positive regulator of ICAM-1 in the TLR4/LPS pathway.RNA biology · 2016Article
- Maresin 1 mitigates LPS-induced acute lung injury in mice.British journal of pharmacology · 2014Article
- Vascular targeting of nanocarriers: perplexing aspects of the seemingly straightforward paradigm.ACS nano · 2014Review
- Stat2 loss leads to cytokine-independent, cell-mediated lethality in LPS-induced sepsis.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Critical role of non-muscle myosin light chain kinase in thrombin-induced endothelial cell inflammation and lung PMN infiltration.PloS one · 2013Article
- Real-time imaging reveals endothelium-mediated leukocyte retention in LPS-treated lung microvessels.Microvascular research · 2012Article
- Dynamic factors controlling targeting nanocarriers to vascular endothelium.Current drug metabolism · 2012Review
- Src phosphorylation of endothelial cell surface intercellular adhesion molecule-1 mediates neutrophil adhesion and contributes to the mechanism of lung inflammation.Arteriosclerosis, thrombosis, and vascular biology · 2011Article
- Innate immune function of the adherens junction protein p120-catenin in endothelial response to endotoxin.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
- The differential role of L-selectin and ICAM-1 in Th1-type and Th2-type contact hypersensitivity.The Journal of investigative dermatology · 2010Article
- Targeting antioxidant and antithrombotic biotherapeutics to endothelium.Seminars in thrombosis and hemostasis · 2010Review
Corrections and comments
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Authors and funding
9 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study examined the effectiveness of antisense oligonucleotides targeted to intercellular adhesion molecule-1 (ICAM-1) to inhibit endotoxin-induced upregulation of ICAM-1 and neutrophil emigration and compared the apparent role of ICAM-1 when examined using antisense oligonucleotides, anti-ICAM-1 antibodies, and ICAM-1 mutant mice. Antisense oligonucleotides inhibited upregulation of ICAM-1 mRNA at 4 and 24 h after instillation of endotoxin in a dose-dependent manner. Neutrophil emigration into the alveolar spaces at 24 h was inhibited by 59%, similar to inhibition using the anti-ICAM-1 antibodies 3E2 (58%) and YN1/1 (75%). No inhibition was observed in the ICAM-1 mutant compared to wild-type mice. These data show that antisense oligonucleotides targeted to ICAM-1 inhibit the endotoxin-induced upregulation of ICAM-1 in the lung and are as effective as anti-ICAM-1 antibodies in preventing neutrophil emigration. The incomplete inhibition by either antisense oligonucleotides or antibodies suggests that alternative adhesion pathways that do not require ICAM-1 are important in neutrophil emigration in the lungs. The disparity in the role of ICAM-1 when evaluated using antisense or antibodies compared to mutant mice suggests that either these inhibitors are exerting additional effects on endothelial cells other than blockade of ICAM-1 or mutant mice have upregulated the ICAM-1-independent pathways to compensate for the long-term loss of ICAM-1.
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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.