scholarly journals Dietary fish oil enhances adhesion molecule and interleukin-6 expression in mice with polymicrobial sepsis

2006 ◽  
Vol 96 (5) ◽  
pp. 854-860 ◽  
Author(s):  
Chun-Sen Hsu ◽  
Wan-Chun Chiu ◽  
Chiu-Li Yeh ◽  
Yu-Chen Hou ◽  
Szu-Yuan Chou ◽  
...  
Keyword(s):  
Fish Oil ◽  
Adhesion Molecule ◽  
Neutrophil Infiltration ◽  
Interferon Γ ◽  
Polymicrobial Sepsis ◽  
Intercellular Adhesion Molecule ◽  
Control Group ◽  
Intercellular Adhesion Molecule 1 ◽  
Group 12 ◽  
Dietary Fish

This study investigated the effects of fish oil (FO) diet on plasma intercellular adhesion molecule 1 (ICAM-1) levels and leucocyte integrin expression in polymicrobial sepsis. Mice were randomly assigned to a control group and an FO group. The control group was fed a medium-fat diet containing soyabean oil, whereas in the FO group, 70 % of the soyabean oil was replaced by FO for 3 weeks. After that, sepsis was induced by caecal ligation and puncture (CLP) in the experimental groups and mice were killed at 0, 6, 12 and 24 h, respectively, after CLP. Results showed that compared with the control group, plasma ICAM-1 levels were higher in the FO group 6 h after CLP. Intra-lymphocyte interferon-γ expression in the FO group was lower, whereas IL-4 expression was higher than in the control group 12 and 24 h after CLP. The expression of leucocyte integrin was significantly higher in the FO group 12 and 24 h after CLP. The FO group had higher IL-6 levels at 12 h in the lungs, at 6 and 12 h in the kidneys, and at 6, 12 and 24 h in the intestines after CLP. The survival rate did not differ between the two groups after CLP. The present findings suggest that pretreatment with an FO diet enhances adhesion molecule and inflammatory cytokine expressions during sepsis, which might aggravate the inflammatory reaction and increase neutrophil infiltration into tissues. In addition, FO diet promotes the Th2-type response and suppresses cellular immune response in polymicrobial sepsis.

scholarly journals Interleukin-10 Inhibits Interferon-γ–Induced Intercellular Adhesion Molecule-1 Gene Transcription in Human Monocytes

Blood ◽  
1997 ◽  
Vol 89 (12) ◽  
pp. 4461-4469 ◽  
Author(s):  
Seng Song ◽  
Hsiang Ling-Hu ◽  
Kenneth A. Roebuck ◽  
Mohammed F. Rabbi ◽  
Raymond P. Donnelly ◽  
...  
Keyword(s):  
Tyrosine Phosphorylation ◽  
Gene Transcription ◽  
Adhesion Molecule ◽  
Interleukin 10 ◽  
Interferon Γ ◽  
Intercellular Adhesion ◽  
Intercellular Adhesion Molecule ◽  
Human Monocytes ◽  
Intercellular Adhesion Molecule 1 ◽  
Ifn Γ

Abstract Interleukin-10 (IL-10) is a potent monocyte regulatory cytokine that inhibits gene expression of proinflammatory mediators. In this study, we investigated the mechanism by which IL-10 downregulates expression of intercellular adhesion molecule-1 (ICAM-1) on the cell surface of normal human monocytes activated with interferon-γ (IFN-γ). IL-10 inhibition of IFN-γ–induced ICAM-1 expression was apparent as early as 3 hours and was blocked by an anti–IL-10 antibody but not by an isotype-matched control antibody. Northern blot analysis showed that IL-10 reduced the accumulation of ICAM-1 mRNA in IFN-γ–stimulated monocytes. IL-10 inhibition of ICAM-1 steady-state mRNA was detected at 3 hours and remained at 24 hours. Nuclear run-on transcription assays showed that IL-10 inhibited the rate of IFN-γ–induced transcription of the ICAM-1 gene, and mRNA stability studies showed that IL-10 did not alter the half-life of IFN-γ–induced ICAM-1 message. Thus, IL-10 inhibits IFN-γ–induced ICAM-1 expression in monocytes primarily at the level of gene transcription. Activation of IFN-γ–responsive genes requires tyrosine phosphorylation of the transcriptional factor STAT-1α (signal transducer and activator of transcription-1α). However, IL-10 did not affect IFN-γ–induced tyrosine phosphorylation of STAT-1α or alter STAT-1α binding to the IFN-γ response element (IRE) in the ICAM-1 promoter. Instead, IL-10 prevented IFN-γ–induced binding activity at the NF-κB site of the tumor necrosis factor α (TNF-α)–responsive NF-κB/C-EBP composite element in the ICAM-1 promoter. These data indicate that IL-10 inhibits IFN-γ–induced transcription of the ICAM-1 gene by a regulatory mechanism that may involve NF-κB.

Endothelial Function in Patients with Severe and Moderate Haemophilia A and B

2018 ◽  
Vol 39 (02) ◽  
pp. 195-202
Author(s):  
Stephanie Böhmert ◽  
Ralf Schubert ◽  
Stephan Fichtlscherer ◽  
Sonja Alesci ◽  
Wolfgang Miesbach
Keyword(s):  
Endothelial Function ◽  
Adhesion Molecule ◽  
Reactive Hyperemia ◽  
Intercellular Adhesion Molecule ◽  
Control Group ◽  
Low Grade ◽  
Haemophilia A ◽  
Intercellular Adhesion Molecule 1 ◽  
Age Related ◽  
Artery Disease

AbstractThe life expectancy of patients with haemophilia has increased and therefore the interest in age-related comorbidities has grown. The aim of this study was to determine whether haemophilia patients have a different endothelial function compared with the general population. A total of 26 patients with severe or moderate haemophilia A or B, 14 controls and 36 patients with coronary artery disease (CAD) were included in this study. Five markers of endothelial dysfunction (MOEDs) were determined. Moreover, the endothelial function was examined using the Itamar Endo-PAT, and the reactive hyperemia index (RHI) was calculated from the results. The MOEDs soluble intercellular adhesion molecule-1 (p = 0.0095) and interleukin-6 (p = 0.010) were significantly higher for patients with haemophilia compared with the control group. The presence of increased adhesion molecule levels and low-grade inflammation is suggestive of a decreased endothelial function. RHI is impaired in CAD patients (1.862), whereas haemophilia patients have an RHI of 1.958 in comparison with 2.112 in controls (p = 0.127). Therefore, laboratory and functional measurements imply a possible higher risk for CAD in haemophilia patients.

Relationship between intercellular adhesion molecule-1 and morbidly adherent placenta

2018 ◽  
Vol 47 (1) ◽  
pp. 45-49
Author(s):  
Engin Korkmazer ◽  
Rampia Nizam ◽  
Emine Arslan ◽  
Özgür Akkurt
Keyword(s):  
Adhesion Molecule ◽  
Histochemical Staining ◽  
Uterine Wall ◽  
Intercellular Adhesion ◽  
Intercellular Adhesion Molecule ◽  
Control Group ◽  
Positive Staining ◽  
Intercellular Adhesion Molecule 1 ◽  
Morbidly Adherent Placenta ◽  
Adherent Placenta

Abstract Objective Morbidly adherent placenta (MAP) is a clinical condition the prevalance of which is steadily increasing. It is described as the invasion of the placenta into the uterine wall through the myometrium and beyond. Several studies have shown that intercellular adhesion molecule-1 (ICAM-1) increases the invasion capability of tumor cells and placental cells. In our study, we investigated the expression of ICAM-1 in MAP cases. Methods This is a prospective case-control study. Eighty-nine patients who were diagnosed with MAP and 96 patients, without adherent placenta, as a control group were included in the study. ICAM-1 staining was examined by immuno-histochemical staining in placental samples. Results Of the 89 patients in the MAP group, 72 (80.8%) showed positive staining, while 26 (27%) did so in the control group. ICAM-1 positive staining in the MAP group was statistically significantly higher (P=0.03). Conclusion This is the first study investigating the relationship between MAP and ICAM-1 in the literature. In our study, we showed that ICAM-1 expression increased in the MAP group.

scholarly journals Eosinophil adhesion to cholinergic nerves via ICAM-1 and VCAM-1 and associated eosinophil degranulation

2002 ◽  
Vol 282 (6) ◽  
pp. L1279-L1288 ◽  
Author(s):  
Deborah A. Sawatzky ◽  
Paul J. Kingham ◽  
Emma Court ◽  
Bharathy Kumaravel ◽  
Allison D. Fryer ◽  
...  
Keyword(s):  
Adhesion Molecules ◽  
Adhesion Molecule ◽  
Primary Cultures ◽  
Specific Inhibitor ◽  
Interferon Γ ◽  
Intercellular Adhesion Molecule ◽  
Cholinergic Nerves ◽  
Intercellular Adhesion Molecule 1 ◽  
Functional Studies

In vivo, eosinophils localize to airway cholinergic nerves in antigen-challenged animals, and inhibition of this localization prevents antigen-induced hyperreactivity. In this study, the mechanism of eosinophil localization to nerves was investigated by examining adhesion molecule expression by cholinergic nerves. Immunohistochemical and functional studies demonstrated that primary cultures of parasympathetic nerves express vascular cell adhesion molecule-1 (VCAM-1) and after cytokine pretreatment with tumor necrosis factor-α and interferon-γ intercellular adhesion molecule-1 (ICAM-1). Eosinophils adhere to these parasympathetic neurones after cytokine pretreatment via a CD11/18-dependent pathway. Immunohistochemistry and Western blotting showed that a human cholinergic nerve cell line (IMR-32) expressed VCAM-1 and ICAM-1. Inhibitory experiments using monoclonal blocking antibodies to ICAM-1, VCAM-1, or CD11/18 and with the very late antigen-4 peptide inhibitor ZD-7349 showed that eosinophils adhered to IMR-32 cells via these adhesion molecules. The protein kinase C signaling pathway is involved in this process as a specific inhibitor-attenuated adhesion. Eosinophil adhesion to IMR-32 cells was associated with the release of eosinophil peroxidase and leukotriene C4. Thus eosinophils adhere to cholinergic nerves via specific adhesion molecules, and this leads to eosinophil activation and degranulation; this may be part of the mechanism of eosinophil-induced vagal hyperreactivity.

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