ArticleMediators of inflammation2014
Blockade of ICAM-1 improves the outcome of polymicrobial sepsis via modulating neutrophil migration and reversing immunosuppression.
Article in Mediators of inflammation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 35 citations in OpenAlex.
- Unraveling NETs in Sepsis: From Cellular Mechanisms to Clinical Relevance.International journal of molecular sciences · 2025Review
- Dimethyl fumarate attenuates liver injury in a mouse model of cecal ligation and puncture by modulating inflammatory, angiogenic and pyroptotic pathways.BMC pharmacology & toxicology · 2025Article
- Plasma Soluble Intercellular Adhesion Molecule-1 Has a Central Role in Biomarker Network Analysis and Is Associated With Poor Outcomes in Two Distinct Pediatric Cohorts of Acute Respiratory Distress Syndrome and Acute Respiratory Failure.Critical care medicine · 2025Article
- ICAM-1/CD18-mediated sequestration of parasitized phagocytes in cortical capillaries promotes neuronal colonization by Toxoplasma gondii.Nature communications · 2025Article
- The Need for Standardized Guidelines for the Use of Monocyte Distribution Width (MDW) in the Early Diagnosis of Sepsis.Journal of personalized medicine · 2024Review
- Applications of peptides in nanosystems for diagnosing and managing bacterial sepsis.Journal of biomedical science · 2024Review
- From immune dysregulation to organ dysfunction: understanding the enigma of Sepsis.Frontiers in microbiology · 2024Review
- Targeting VEGF using Bevacizumab attenuates sepsis-induced liver injury in a mouse model of cecal ligation and puncture.Journal of medicine and life · 2023Article
- The implication of targeting PD-1:PD-L1 pathway in treating sepsis through immunostimulatory and anti-inflammatory pathways.Frontiers in immunology · 2023Review
- Neutrophil reverse migration.Journal of inflammation (London, England) · 2022Review
- Cyclooxygenase-2 deficiency attenuates lipopolysaccharide-induced inflammation, apoptosis, and acute lung injury in adult mice.American journal of physiology. Regulatory, integrative and comparative physiology · 2022Article
- Pharmacological Inhibition of FAK-Pyk2 Pathway Protects Against Organ Damage and Prolongs the Survival of Septic Mice.Frontiers in immunology · 2022Article
- Transcriptomic Analysis Reveals Differential Expression of Genes between Lung Capillary and Post Capillary Venules in Abdominal Sepsis.International journal of molecular sciences · 2021Article
- Therapeutic Potential of Extracellular Vesicles for Sepsis Treatment.Advanced therapeutics · 2021Article
- Frontline Science: The expression of integrin αJournal of leukocyte biology · 2021Article
- Murine Myeloid Progenitors Attenuate Immune Dysfunction Induced by Hemorrhagic Shock.Stem cell reports · 2021Article
- Macrophage ICAM-1 functions as a regulator of phagocytosis in LPS induced endotoxemia.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021Article
- The effects of sepsis on endothelium and clinical implications.Cardiovascular research · 2021Article
- Inactivation of the tyrosine phosphatase SHP-2 drives vascular dysfunction in Sepsis.EBioMedicine · 2019Article
- DAMPs and NETs in Sepsis.Frontiers in immunology · 2019Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intercellular adhesion molecule-1 (ICAM-1) is a key adhesion molecule mediating neutrophil migration and infiltration during sepsis. But its role in the outcome of sepsis remains contradictory. The current study was performed to investigate the role of anti-ICAM-1 antibody in the outcome of polymicrobial sepsis and sepsis-induced immune disturbance. Effect of anti-ICAM-1 antibody on outcome of sepsis induced by cecal ligation and puncture (CLP) was evaluated by the survival analysis, bacterial clearance, and lung injury. Its influence on neutrophil migration and infiltration, as well as lymphocyte status, in thymus and spleen was also investigated. The results demonstrated that ICAM-1 mRNA was upregulated in lung, thymus, and spleen of CLP mice. Anti-ICAM-1 antibody improved survival and bacterial clearance in CLP mice and attenuated lung injury. Migration of neutrophils to peritoneal cavity was enhanced while their infiltration into lung, thymus, and spleen was hampered by ICAM-1 blockade. Anti-ICAM-1 antibody also prevented sepsis-induced apoptosis in thymus and spleen. Positive costimulatory molecules including CD28, CD80, and CD86 were upregulated, while negative costimulatory molecules including PD-1 and PD-L1 were downregulated following anti-ICAM-1 antibody administration. In conclusion, ICAM-1 blockade may improve outcome of sepsis. The rationale may include the modulated neutrophil migration and the reversed immunosuppression.
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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.