Changes In Intercellular Adhesion Molecule-1 Research Articles

Association of Endothelial Cell Activation with Acute Kidney Injury during Coronary Angiography and the Influence of Recombinant Human C1 Inhibitor-A Secondary Analysis of a Randomized, Placebo-Controlled, Double-Blind Trial.

Acute kidney injury (AKI) as a result of iodinated contrast media (CM) has been linked to CM-induced renal ischemia and toxic effects on endothelial cells (EC). The recombinant human C1 inhibitor (rhC1INH) has been shown to influence EC activation. Secondary analysis of 74/77 (96%) participants of a double-blind, randomized, and placebo-controlled study that assessed the effect of rhC1INH on AKI. E-selectin, intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule (VCAM-1), and CC-chemokin-ligand-5 (CCL5) were determined in frozen blood samples over 48 h and analyzed according to the treatment group and renal outcomes. The mean age was 76.7 years, and 37 patients each received rhC1INH and placebo, respectively. In the entire study population, minor differences in median EC activation markers/CCL5 concentrations during the first 48 h compared to baseline were observed (e.g., E-selectin 27.5 ng/mL at baseline vs. 29.7 ng/mL on day 1, CCL5: 17.7 ng/mL at baseline vs. 32.2 ng/mL on day 2). Absolute changes in ICAM-1/E-selectin concentrations correlated with a higher peak change in urinary NGAL concentrations. However, AKI was not associated with significant changes in EC markers/CCL5. Last, no significant differences in serum concentrations of EC activation markers/CCL5 were evident between the placebo and the rhC1INH group. CM administration during coronary angiography only mildly activated ECs within the first 48 h, which does not explain subsequent AKI. The administration of rhC1INH was not associated with a reduction of EC activation or CCL5.

Influence of cardiorespiratory training program on the intercellular adhesion molecule level in patients with postmastectomy syndrome

To evaluate the influence of 12-week aerobic dynamic training program of moderate intensity on the endothelial dysfunction laboratory markers and life quality in patients with PMS. Single-center prospective randomized trial included 40 patients with PMS divided into study (20 patients) and comparative (20 patients) groups, as well as 20 healthy female volunteers. The expression level of soluble intercellular adhesion molecule-1 (ICAM-1) and platelet endothelial cell adhesion molecule-1 (PECAM-1) were evaluated in all participants at baseline by enzyme-linked immunosorbent assay method, and additionally psychological and physical component of health by SF-36 questionnaire were assessed in patients with PMS. The group of patients with PMS after BC treatment had increased level of ICAM-1 in long-term period, that may indicate endothelial dysfunction. Statistically significant decrease of endothelial dysfunction laboratory markers was revealed in patients with PMS, who underwent the course of cardiorespiratory training. In the same time, the dynamics of changes in ICAM-1 was higher in the study group than in comparative group. Further, improvement of physical and psychological components of health by SF-36 questionnaire was found. The program of cardiorespiratory trainings of moderate intensity in patients, who had BC treatment a year ago, decreases intercellular adhesion molecules level that may show an improvement of endothelial dysfunction.

Metabolic Abnormalities, Inflammatory Markers and Endothelial Dysfunction in Hyperprolactinemia due to Prolactinoma before and after Normalization of Serum Prolactin: A Prospective Case Control Study.

Hyperprolactinemia is associated with obesity, dyslipidemia, insulin resistance, and low-grade inflammation which may promote endothelial dysfunction (EnD). Limited work has been done on EnD in prolactinomas and we, therefore, studied serum markers of inflammation and EnD in patients with prolactinomas before and after treatment with dopamine agonists. Fifty-six treatment naïve patients with prolactinomas and fifty-three (apparently healthy age and sex-matched) controls were enrolled in the study and subjected to clinical assessment and laboratory investigations including blood glucose, total cholesterol, triglycerides, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, urea, creatinine, uric acid, erythrocyte sedimentation rate (ESR), highly sensitive C-reactive protein (hsCRP) and markers of EnD i.e., intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1). Patients were treated with a dopamine agonist (cabergoline) and parameters (like ESR, hsCRP, ICAM-1, and VCAM-1) were measured at 12 weeks. The majority of the patients (84%) were female, more than half (52%) had metabolic syndrome and over a third (36%) were obese. Blood glucose fasting, HbA1c, lipid fractions, ESR, hsCRP, ICAM-1, and VCAM-1 were significantly higher in patients than in controls. Median ICAM-1 was 1331.95 ng/ml (IQR 803.43-1825.99) in patients vs 753.04 ng/ml (IQR 402.04-871.55) in controls, P < 0.001 and median VCAM-1in patients was 971.35 ng/ml (IQR 695.03-1285.23) as against 634.56 ng/ml (IQR 177.49-946.50) in controls, p0.001. Serum ICAM-1 and VCAM-1 correlated positively with hsCRP. On multivariate regression analysis, serum hsCRP was the only significant predictor of change in ICAM-1 and VCAM-1. Normalization of serum PRL with CAB resulted in a significant decrease in metabolic parameters, ESR, hsCRP, ICAM-1, and VCAM-1. Hyperprolactinemia because of prolactinoma is associated with EnD secondary to systemic inflammation and metabolic abnormalities which improve after treatment with DA.

Changes in sleepiness and 24-h blood pressure following 4 months of CPAP treatment are not mediated by ICAM-1.

Continuous positive airway pressure (CPAP) therapy reduces circulating intercellular adhesion molecule 1 (ICAM-1) in adults with obstructive sleep apnea (OSA). ICAM-1 levels may affect the daytime sleepiness and elevated blood pressure associated with OSA. We evaluated the association of changes from baseline in ICAM-1 with changes of objective and subjective measures of sleepiness, as well as 24-h ambulatory blood pressure monitoring (ABPM) measures, following 4 months of CPAP treatment. The study sample included adults with newly diagnosed OSA. Plasma ICAM-1, 24-h ABPM, Epworth Sleepiness Scale (ESS), and psychomotor vigilance task (PVT) were obtained at baseline and following adequate CPAP treatment. The associations between changes in natural log ICAM-1 and changes in the number of lapses on PVT, ESS score, and 24-h mean arterial blood pressure (MAP) were assessed using multivariate regression models, controlling for a priori baseline covariates of age, sex, BMI, race, site, smoking status, physical activity, anti-hypertensive medications, AHI, and daily hours of CPAP use. Among 140 adults (83% men),mean (± SD) body mass index (BMI) was 31.5± 4.2 kg/m2, and apnea-hyopnea index (AHI) was 36.8± 15.3 events/h.Sleepiness measures, although not ICAM-1 or ABPM measures, improved significantly following CPAP treatment. We observed no statistically significant associations between the change in ICAM-1 and changes in sleepiness, MAP, or other ABPM measures. Changes in ICAM-1 levels were not related to changes in sleepiness or ABPM following CPAP treatment of adults with OSA. Future work should explore whether or notother biomarkers may have a role in mediating these treatment outcomes in adults with OSA.

0053 Effect of Changes in Intracellular Adhesion Molecule-1 on Measures of Sleepiness and 24-hour Ambulatory Blood Pressure After 4 Months of Continuous Positive Airway Pressure

Abstract Introduction Previous studies have shown that continuous positive airway pressure (CPAP) therapy of adults with obstructive sleep apnea (OSA) reduces circulating levels of intercellular adhesion molecule 1 (ICAM-1). ICAM-1 levels may affect daytime sleepiness and elevated blood pressure associated with OSA. Our goals were to explore associations between changes in ICAM-1 and objective and subjective measures of sleepiness, as well as 24-hour ambulatory blood pressure monitor (ABPM) parameters in adults with OSA following 4 months of CPAP treatment. Methods We identified 140 adults with newly diagnosed OSA in the Penn Icelandic Sleep Apnea (PISA) Study, with a mean (±SD) body mass index (BMI) of 31.5±4.2 kg/m2 and apnea-hypopnea index (AHI) of 36.8±15.3 events/hour; 83.3% were males. Plasma ICAM-1 levels, 24-hour ABPM, Epworth Sleepiness Scale (ESS), and Psychomotor Vigilance Task (PVT) measures were obtained at baseline and after 4 months of CPAP treatment. Associations between changes in natural log ICAM-1 and both sleepiness and 24-hour mean arterial blood pressure (MAP) were assessed using multivariate regression models, controlling for a priori baseline covariates of age, sex, BMI, race, site, smoking status, physical activity, use of anti-hypertensive medications, AHI and hours/night of CPAP usage. Results Overall, there was no significant change in ICAM-1 from baseline to follow-up among all participants after 4 months (0.027 ng/ml, p=0.52). There were no statistically significant associations between the change in ICAM-1 and change in sleepiness measures (all p&amp;gt;0.05) or 24-hour MAP (1.124 mm Hg, p=0.07). A nominal association between increased ICAM-1 and increased daytime MAP after 4 months was observed (1.39 mm Hg, p=0.033), although this result was not significant after correction for multiple comparisons. Conclusion Our results do not support changes in ICAM-1 as the biological pathway linking changes in sleepiness or ABPM following CPAP treatment of adults with OSA. Support P01-HL094307 (NHLBI, PI: Pack AI)

Changes in Expressions of Bcl-2, Inflammatory Factors IL-1, IL-6 and IL-8 and Intercellular Adhesion Molecule-1 in Inflammatory Dental Pulp

Background: To investigate the expressional changes of intercellular adhesion molecule-1 (ICAM-1), B-cell lymphoma/leukemia-2 (Bcl-2) and inflammatory factors [interleukin-1 (IL-1), IL-6 and IL-8] in the inflammatory dental pulp. Methods: 70 patients from June 2017 to May 2018 were selected as the research objects. The levels of ICAM-1, Bcl-2, IL-1, IL-6, IL-8 and in the third molars were detected and compared between healthy people and patients with acute and chronic pulpitis. Results: We found weak positive result regarding Bcl-2 and ICAM-1 expressions in normal dental pulp, while positive signal was enhanced in chronic pulpitis, and strongly positive was found in acute pulpitis. The expressions of inflammatory factors IL-1, -6, -8 in normal dental pulp were significantly lower than those in dental pulp with acute and chronic inflammations (p &lt; 0.05). The inflammatory factors levels in dental pulp with chronic inflammation were significantly decreased compared with those in dental pulp with acute inflammation (p &lt; 0.05). Conclusion: Bcl-2 and ICAM-1 cause the occurrence of inflammatory dental pulp, along with the abnormal increase of IL-1, IL-6 and IL-8.

Intercellular adhesion molecule-1 and S-100β in sevoflurane combined with epidural anesthesia for radical resection of lung cancer.

Significance of intercellular adhesion molecule-1 (ICAM-1) and S-100β protein (S-100β) were investigated in sevoflurane combined with epidural anesthesia for radical resection of lung cancer. In total, 172 patients who underwent radical resection of lung cancer from May 2014 to January 2016 and 160 blood samples from healthy patients in the same period were selected for prospective analysis. Lung cancer patients were the therapy group (TG). Venous blood (2 ml) was taken from patients before anesthesia (T1) and after anesthesia at 30 min (T2), 3 h (T3) and 24 h (T4), respectively. Healthy physical examination samples were the control group (CG). Enzyme linked immunosorbent assay (ELISA) was used to detect the concentration of ICAM-1 and RT-PCR to detect the concentration of S-100β. The changes of ICAM-1 and S-100β concentrations and their significance to patients were analyzed. The serum ICAM-1 and S-100β concentrations in TG were significantly higher than those in CG (P<0.001), and were the highest at T1 (P>0.001), followed by T2 (P<0.001). Of the 172 patients 27 cases had adverse complications during the perioperative period. Patients were divided into the ICAM-1 high concentration group (CHCG), the ICAM-1 low concentration group (CLCG) and the S-100β high concentration group (SHCG) and the S-100β low concentration group (SLCG). The 3-year survival rate of CHCG was significantly lower than CLCG and SLCG (P<0.001). ICAM-1 and S-100β protein in sevoflurane combined with epidural anesthesia for radical resection of lung cancer can effectively predict the perioperative adverse complications of patients, and have better monitoring significance for the prognosis of patients.

Screening the anti-gout traditional herbs from TCM using an in vitro method

The aim of this work was to evaluate the ability of 33 herbal extracts in inhibiting the acute inflammation and xanthine oxidase (XOD) activity. The anti-inflammation effects of the herbal extracts were detected by an in vitro cell model, which was established by stimulating human umbilical vein endothelial cells (HUVEC) using sodium urate (MSU). In this model, the intercellular adhesion molecule-1 (ICAM-1) and interleukin-1 beta (IL-1β) were expressed, and the anti-inflammation effects of herbal extracts were evaluated by detecting the content changes of ICAM-1 and IL-1β in cell lysates and cell culture supernates using an enzyme-linked immunosorbent assay (ELISA). Moreover, an ultrahigh performance liquid chromatography and tandem mass spectrometry (UPLC–MS/MS) method was used for the detection of XOD activity and the screening of XOD inhibitors in this research. The amount of uric acid from each analyte was directly detected using the multiple reaction monitoring mode and the uric acid level could be reduced via the addition of an inhibitor. Results indicated that Salviae Miltiorrhizae Radix et Rhizome, Rhei Radix et Rhizoma, Polygoni Cuspidati Rhizoma et Radix, Selaginellae Herba, Paeoniae Radix Rubra, especially Ginkgo Folium seemed to be more effective in anti-inflammation and inhibiting XOD activity. The anti-inflammation and enzyme inhibitory activities of the herbal extracts may be correlated with their bioactive components. And the differences between the herbal extracts were correlated with the amount of flavonoid and anthraquinone components. In our study, we have investigated the potential anti-inflammation bioactivity of 33 herbal extracts in vitro, which could provide a reference for further in vivo research in the prevention and treatment of gout.

Fine particles, genetic pathways, and markers of inflammation and endothelial dysfunction: Analysis on particulate species and sources.

Studies have found associations between PM2.5 and cardiovascular events. The role of different components of PM2.5 is not well understood. We used linear mixed-effects models with the adaptive LASSO penalty to select PM2.5 species and source(s), separately, that may be associated with markers of inflammation and endothelial dysfunction, with adjustment for age, obesity, smoking, statin use, diabetes mellitus, temperature, and season as fixed effects in a large longitudinal cohort of elderly men. We also analyzed these associations with source apportionment models and examined genetic pathway-air pollution interactions within three relevant pathways (oxidative stress, metal processing, and endothelial function). We found that independent of PM2.5 mass vanadium (V) was associated with intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1). An IQR increase (3.2 ng/m(3)) in 2-day moving average V was associated with a 2.5% (95% CI: 1.2-3.8%) change in ICAM-1 and a 3.9% (95% CI: 2.2-5.7%) change in VCAM-1, respectively. In addition, an oil combustion source rich in V was linked to these adhesion molecules. People with higher allelic risk profiles related to oxidative stress may have greater associations (P-value of interaction=0.11). Our findings suggest that particles derived from oil combustion may be associated with inflammation and endothelial dysfunction, and it is likely that oxidative stress plays a role in the associations.

Silencing of PKC-α, TRPC1 or NF-κB expression attenuates cisplatin-induced ICAM-1 expression and endothelial dysfunction

Platinum-based chemotherapy has been associated with increased long-term cardiovascular events. Also noteworthy is the accumulating awareness of early vascular toxicity occurring at the time of chemotherapy or immediately thereafter. The objective of the study was to delineate the molecular mechanisms associated with the early vascular toxicity and test the molecular silencing approach towards attenuating the endothelial dysfunction during platinum-based chemotherapy. Human umbilical vein endothelial cells (HUVECs) were treated with varying concentrations of cisplatin (1.0–10.0μg/ml) or vehicle control (0.1% dimethyl sulfoxide) for monitoring the changes in Intercellular adhesion molecule-1 (ICAM-1) mRNA and protein expression viz. a viz. altered activation of protein kinase C (PKC) isoforms, transient receptor potential channel (TRPC) 1 expression, Nuclear factor ‘kappa-light-chain-enhancer’ of activated B-cells (NF-κB), Store Operated Ca2+ Entry (SOCE) in cisplatin-induced endothelial permeability and adherence of the activated endothelial cells to human monocyte-like U937 cells. Silencing of either PKC-α, TRPC1 or p65 subunit of NF-κB, all resulted in significant alleviation of cisplatin-induced endothelial dysfunction. At concentrations ≥8μg/ml, cisplatin induced a significant increase in the expression of ICAM-1 mRNA as well as protein. This was mediated by changes in PKC-α membrane translocation, NF-κB activation, increased expression as well as phosphorylation of TRPC1 and enhanced SOCE, leading to hyperpermeability and leakage of albumin. Increased adherence of U937 monocytes to cisplatin-activated endothelial cells was evident. Cisplatin challenge activates PKC-α, which in turn phosphorylated TRPC1 resulting in enhanced Ca2+ entry. Increased Ca2+ flux is required for activation of NF-κB and ICAM-1 expression. Enhanced ICAM-1 expression promotes monocyte binding to endothelial cells and increased endothelial hyperpermeability.

PP.07.13

Objective: Pro-inflammatory stimuli and pro-atherogenic factors are known to reduce the level of endothelial-derived netrin-1, a secreted laminin-like protein that attenuates recruitment of circulating monocytes within atherosclerotic plaques. This study investigated the effect of aspirin, routinely used for the prevention of cardiovascular disease, on serum netrin-1 levels in healthy subjects. Design and method: Serum netrin-1 was measured using an enzyme-linked immunosorbent assay (ELISA) in samples collected from 60 subjects before and after 28 days of treatment with 300 mg aspirin daily. ELISAs were performed to assess serum levels of intercellular adhesion molecule-1 (ICAM-1), E-selectin, and urinary 11-dehdyro-thromboxane B2 levels (TXB2). Serum creatinine and salicylate levels were measured using the creatininase enzymatic method on a Roche C8000 analyser and a Cobas Fara automated analyser (Roche) respectively. Creatinine clearance was calculated using the Cockcroft-Gault equation. The Research Ethics Committee approved this study and subjects signed consent forms. Results: Serum netrin-1 levels were reduced following aspirin treatment (66.06 ± 22.98pg/ml versus 79.79 ± 34.91pg/ml at baseline; p = 0.0022). There was a linear association between the percentage change in netrin-1 and level of serum salicylate (r2 = 0.413, p = 0.0013). TXB2 levels fell in all subjects post-treatment, confirming adherence to treatment (32.99 ± 18.35ng/mmol creatinine versus 143.7 ± 54.25ng/mmol creatinine at baseline; p < 0.0001). Serum ICAM-1 and E-selectin levels were not modified by treatment. Creatinine clearance decreased following aspirin (103.2 ± 26.13 ml/min versus 110.5 ± 26.95 ml/min at baseline; p = 0.0011). Conclusions: This study demonstrates that serum netrin-1 is reduced following treatment with aspirin. The TXB2 measurements show effective platelet inhibition in the whole population. We observed no change in ICAM-1 or E-selectin levels suggestive of an effect on the vascular endothelial function. Netrin-1 is a known biomarker of renal impairment. We propose that the reduction in netrin-1 is secondary to drug-induced renal dysfunction, as evidenced by a decrease in creatinine clearance.

Adhesion molecule increases in sleep apnea: beneficial effect of positive airway pressure and moderation by obesity.

BackgroundElevated levels of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) may contribute to cardiovascular disease and are associated with obstructive sleep apnea (OSA) and obesity. The relationship between OSA and obesity in determining ICAM-1 and VCAM-1 levels, and the effect of treatment, is unclear.ObjectiveOur aim was to study whether positive airway pressure (PAP) usage resulted in changes in ICAM-1 and VCAM-1 after 2 years within 309 OSA patients from the Icelandic Sleep Apnea Cohort, and determine how obesity affected such changes.Subjects/MethodsThe mean body mass index (BMI) was 32.4±5.1 kg/m2; subjects had moderate-to-severe OSA (apnea-hypopnea index = 45.0±20.2) and 79% were male. There were 177 full PAP users (≥4 hours/night and ≥20 of last 28 nights), 44 partial (<4 hours/night or <20 nights), and 88 non-users.ResultsICAM-1 (p<0.001) and VCAM-1 (p=0.012) change was significantly different among the PAP groups. The largest ICAM-1 differences were among the most obese subjects (p<0.001). At follow-up, non-users had increased ICAM-1 compared to decreased levels in full users. All groups had increased VCAM-1, but non-users had a significantly larger increase than full users.ConclusionWithin moderate-to-severe OSA patients, PAP usage prevents increases in adhesion molecules observed in non-users after two years. For ICAM-1, the largest effect is in the most obese subjects. As OSA and obesity commonly coexist, the usage of PAP to limit increases in adhesion molecules may decrease the rate of progression of OSA-related cardiovascular disease.

Exploring molecular mechanism underlying Chinese medicine syndrome: A study on correlation between Chinese medicine syndrome and biomarkers for ischemic stroke

To investigate whether Chinese medicine (CM) syndrome is associated with particular molecular mechanism, we explored the correlation between CM syndrome and changes of intercellular adhesion molecule-1 (ICAM-1), matrix metalloproteinase 9 (MMP-9) and heat shock protein 70 (HSP70) in patients with ischemic stroke, which were reported to play an important role in the inflammatory and apoptosis cascade. CM syndrome factors of 175 patients with ischemic stroke were assessed using Ischemic Stroke CM Syndrome Factor Diagnostic Scale (ISTSFDS). The patients were grouped according to the main syndrome factor combinations at different time points based on distribution probability of syndrome factor combinations. Blood levels of ICAM-1, MMP-9 and HSP70 were quantified by enzyme-linked immunosorbent assay. ICAM-1 expression was significantly higher in the internal-wind+phlegm-dampness+blood-stasis, phlegmdampness+ blood-stasis, internal-fire+phlegm-dampness+blood-stasis group than that in the blood-stasis+qideficiency group within 72 h from stroke onset (P <0.05); HSP70 expression was significantly lower in the phlegm-dampness+blood-stasis, internal-fire+phlegm-dampness+blood-stasis, blood-stasis group than that in the phlegm-dampness+blood-stasis+qi-deficiency group on the 7th day from stroke onset (P<0.05). Phlegm-dampness and blood-stasis exist through the whole process of ischemic stroke. An increased level of ICAM-1 and a reduced level of HSP70 reflect the pathological state of phlegm-stasis mutual binding. These results suggest that inflammation and apoptosis induced by cerebral vascular injury in the pathological processes of ischemic stroke are more prominent in the excess syndrome state like phlegm-dampness and blood-stasis.

Epigenetic upregulation of p66shc mediates low-density lipoprotein cholesterol-induced endothelial cell dysfunction

Hypercholesterolemia characterized by elevation of low-density lipoprotein (LDL) cholesterol is a major risk factor for atherosclerotic vascular disease. p66shc mediates hypercholesterolemia-induced endothelial dysfunction and atheromatous plaque formation. We asked if LDL upregulates endothelial p66shc via changes in the epigenome and examined the role of p66shc in LDL-stimulated endothelial cell dysfunction. Human LDL stimulates human p66shc promoter activity and p66shc expression in human endothelial cells. LDL leads to hypomethylation of two CpG dinucleotides and acetylation of histone 3 in the human p66shc promoter. These two CpG dinucleotides mediate LDL-stimulated p66shc promoter activity. Inhibition or knock down of DNA methyltransferases negates LDL-induced endothelial p66shc expression. p66shc mediates LDL-stimulated increase in expression of endothelial intercellular adhesion molecule-1 (ICAM1) and decrease in expression of thrombomodulin (TM). Mirroring these changes in ICAM1 and TM expression, p66shc mediates LDL-stimulated adhesion of monocytes to endothelial cells and plasma coagulation on endothelial cells. These findings indicate that LDL cholesterol upregulates human endothelial p66shc expression via hypomethylation of CpG dinucleotides in the p66shc promoter. Moreover, they show that LDL-stimulated p66shc expression mediates a dysfunctional endothelial cell surface, with proadhesive and procoagulant features.

Divergent anti-inflammatory effects of different oil acute consumption on healthy individuals

Inter-cellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1) and tumor necrosis factor-α (TNF-α), are implicated in atherogenesis. In addition, several types of oil as part of different types of diet are associated with the initiation of atherosclerosis and consequently with the risk of cardiovascular disease. However, the exact role of oil consumption on vascular inflammation remains unknown. In this parallel study, we assessed the acute effects of extra virgin olive oil, soy oil, corn oil and cod liver oil on circulating soluble(s) forms of adhesion molecules and TNF-α. In all, 67 healthy volunteers were randomized to receive 50 ml of oil. Soluble forms of VCAM-1, ICAM-1 and TNF-α were measured by enzyme-linked immunosorbent assay at baseline and at 3 h post oil consumption. All types of oil had no significant effect on soluble VCAM-1 levels (P=nonsignificant (NS) for all). On the contrary, all oil types decreased ICAM-1 levels (P<0.01). Olive oil (P<0.05), soy oil and cod liver oil (P<0.01 for both) reduced TNF-α levels significantly, in contrast to corn oil, which induced a nonsignificant decrease (P=NS). Moreover, there was a significant correlation between the absolute change in ICAM-1 and TNF-α levels (ρ=0.379, P<0.05), but not between the absolute changes in VCAM-1 and TNF-α levels (ρ=0.019, P=NS). Acute consumption of all types of oil decreased significantly ICAM-1 levels. In addition, olive oil, soy oil and cod liver oil decreased significantly TNF-α levels. Moreover, the absolute change in TNF-α levels was correlated with the absolute change in ICAM-1 levels. These findings indicate that acute consumption of specific types of oil is associated with specific significant anti-inflammatory effects.

Thermal Facilitation of Lymphocyte Trafficking Involves Temporal Induction of Intravascular ICAM‐1

Fever is associated with improved survival, although its beneficial mechanisms are poorly understood. Previous studies indicate that the thermal element of fever augments lymphocyte migration across high endothelial venules (HEVs) of lymphoid organs by increasing the intravascular display of a gatekeeper trafficking molecule, intercellular adhesion molecule-1 (ICAM-1). Here, we evaluated the spatio-temporal relationship between the thermal induction of intravascular ICAM-1 and lymphocyte trafficking. Intravascular ICAM-1 density was quantified by immunofluorescence staining in mice exposed to fever-range whole-body hyperthermia (39.5+/-0.5 degrees C). ICAM-1-dependent lymphocyte trafficking was measured in short-term homing assays. A linear relationship was observed between the duration of heat treatment and intravascular ICAM-1 density in HEVs with maximal responses requiring sustained (i.e., five hours) thermal stress. Circulating lymphocytes were found to sense incremental changes in ICAM-1 on HEVs, such that trafficking is proportional to the intravascular density of ICAM-1. We further identified a hydroxamate-sensitive shedding mechanism that restores ICAM-1 expression to homeostatic levels following the cessation of thermal stress. The time-dependent response to thermal stress indicates that ICAM-1 density governs the efficiency of lymphocyte interactions with HEVs in vivo. These studies highlight the dynamic role of the microcirculation in promoting immune surveillance during febrile inflammatory responses.

Clinical study on effect of garlicin in stabilizing the carotid artery atherosclerotic plaque in patients with primary hypertension and coronary artery disease

To investigate the effect of garlicin in treating carotid artery atherosclerotic plaque (CAAP) in patients with primary hypertension and coronary heart disease (PHT-CHD). Seventy-nine patients with PHT-CHD were randomly divided into the treated group (39 patients) treated with garlicin and fosinopril and the control group (40 patients) treated with fosinopril alone. The change of CAAP was evaluated by high frequency ultrasonic examination every six months, and the changes of intercellular adhesion molecule-1 (ICAM-1) and high sensitive C-reactive protein (hs-CRP) were measured by ELISA, with the observation proceeding for 52 weeks totally. By the end of the experiment, the number of complex plaques, Crouse integrals, intima-media thickness, serum ICAM-1 and hs-CRP were significantly lower in the treated group than those in the control group with significant difference (P < 0.05). Garlicin could stabilize CAAP to a certain extent and shows a definite vascular protective effect in patients with PHT-CHD.

Effects of moderate-intensity exercise training on plasma biomarkers of inflammation and endothelial dysfunction in older patients with type 2 diabetes

Background and aims Some plasma biomarkers of inflammation and endothelial dysfunction have been recently recognized as important cardiovascular risk factors. Currently, there is little information about the effects of aerobic exercise training on these biomarkers in older adults with type 2 diabetes. We have therefore assessed the effects of a twice-weekly moderate, aerobic exercise programme, without a concomitant weight loss diet, on plasma inflammatory and endothelial dysfunction biomarkers in older type 2 diabetic patients. Methods and results A group of 16 sedentary, overweight, non-smoking, older patients with type 2 diabetes volunteered to participate in a 6-month, supervised, progressive, aerobic training study, two times per week. Plasma levels of hs-C-reactive protein (hs-CRP), soluble tumour necrosis factor (TNF)-α receptors, P-selectin and intercellular adhesion molecule-1 (ICAM-1) were measured before and after physical training. While hs-CRP and soluble TNF-α receptors remained essentially unaffected by physical training, plasma concentrations of P-selectin ( P < 0.001) and ICAM-1 ( P < 0.01) markedly decreased; physical training also increased HDL cholesterol by 12% ( P < 0.05) and decreased uric acid levels by ∼33% ( P = 0.021). Body weight, waist circumference, blood pressure, haemoglobin A1c, plasma triglyceride and LDL cholesterol concentrations did not change. Interestingly, the exercise-induced changes in ICAM-1 and P-selectin levels remained significant after adjustment for the percent variations of body weight, waist circumference, haemoglobin A1c, HDL cholesterol and uric acid concentrations. Conclusions A twice-weekly, 6-month, progressive aerobic-training programme, without a concomitant weight loss diet, is associated with significant decreases in circulating P-selectin and ICAM-1 levels and with a less atherogenic lipid profile in overweight, non-smoking, older type 2 diabetic individuals.

Effects of candesartan cilexetil and enalapril on inflammatory markers of atherosclerosis in hypertensive patients with non-insulin-dependent diabetes mellitus

Circulating adhesion molecules may have a prognostic significance as markers of endothelial damage. Drugs which inhibit the renin-angiotensin system may be effective in reducing circulating or tissue adhesion molecules, albeit data available are scarce. The aim of the study was to investigate the effects of an angiotensin-converting enzyme (ACE) inhibitor, enalapril and a highly selective angiotensin receptor blocker, candesartan cilexetil, on circulating adhesion molecules in a large sample of patients with non-insulin-dependent diabetes mellitus (NIDDM). The study was comparative, multicenter, randomized and double blind, with two parallel groups. NIDDM patients with a diagnosis of mild (grade 1) essential hypertension were included in the study, at the end of a 2-week placebo run-in period. The primary end-point of the study was to evaluate changes of intercellular adhesion molecule-1 (ICAM-1) plasma levels during treatment. The secondary end-points were: changes in vascular cells adhesion molecule-1 (VCAM-1), von Willebrand factor (vWF), fibrinogen and plasminogen activator inhibitor-1 (PAI-1) circulating levels and of urinary albumin excretion rate (AER) as well; 129 patients were randomized: 66 in the candesartan group and 63 in the enalapril group, 118 of them completed the scheduled 24-week treatment period. Candesartan and enalapril equally reduced circulating level of ICAM-1 and exerted comparable effects on changes of other adhesion molecules and coagulation factors. A similar blood pressure-lowering effect was observed with the two drugs (candesartan: from 148/90 +/- 11/8 to 132/82 +/- 12/7 mmHg, P < 0.01, enalapril: from 148/91 +/- 12/8 to 131/85 +/- 14/6 mmHg, P < 0.01). Candesartan was more effective than enalapril in the reduction of albuminuria (P < 0.05 between treatments), although urinary protein excretion can be considered normal in the majority of patients. The two drugs were comparable in terms of adverse events reported. Candesartan and enalapril showed similar effects on blood pressure and on circulating adhesion molecules. In this study urinary protein excretion was reduced more by candesartan.

The differential expression of intercellular adhesion molecule-1 (ICAM-1) and regulation by interferon-gamma during the pathogenesis of endometriosis.

To establish an in vitro culture model of the endometrium and endometriotic lesions, and demonstrate the different expressions of intercellular adhesion molecule-1 (ICAM-1) in these lesions. Eight women with moderate to severe stages of endometriosis were enrolled. The specimens were collected from their eutopic endometrium, visually normal peritoneum, ovarian endometrioma and peritoneal endometriotic spots during the follicular phase of the menstrual cycle. ICAM-1 mRNA and protein were expressed by using reverse transcription-polymerase chain reaction, enzyme-linked immunosorbent assay, immunoblot, and immunocytochemistry. The results demonstrate that visually normal peritoneal cells and ovarian endometriomas of endometriotic patients can express high ICAM-1 mRNA. Normal peritoneal cells further expressed significant soluble ICAM-1 protein levels without cytokine stimulation. The eutopic endometrium expressed less soluble ICAM-1 protein, and ICAM-1 expressions increased in cultured stromal cells of eutopic endometrium, ovarian endometrioma, and peritoneal endometriotic spots under interferon-gamma (INF-gamma) stimulation. The ICAM-1 expression in visually normal peritoneal cells from women with endometriosis may play a role in the early implantation of peritoneal endometriosis. Peritoneal INF-gamma stimulation is significantly associated with ICAM-1 expression in endometriosis. Therefore, the differential expression and changes of ICAM-1 may be involved in the mechanism that can escape immunosurveillance and allow refluxed endometrial cells to spread and invade other location.