Cell Adhesion Molecules In Patients Research Articles

Effects of Continuous Positive Airway Pressure on Cell Adhesion Molecules in Patients with Obstructive Sleep Apnea: A Meta-Analysis.

Previous studies have confirmed that patients with obstructive sleep apnea (OSA) have higher systemic inflammatory markers, including intercellular adhesion molecule-1(ICAM-1), vascular cell adhesion molecule-1(VCAM-1), and E-selectin compared to control subjects. However, the effects of continuous positive airway pressure (CPAP) therapy on circulating levels of ICAM-1, VCAM-1, and E-selectin in OSA patients remain inconsistent. Therefore, the primary purpose of the present meta-analysis is to estimate the effect of CPAP therapy on these cell adhesion molecules (CAMs) in patients with OSA. The PubMed, Scopus, Embase, and Cochrane Library databases were searched. The overall effects were measured by the standardized mean difference (SMD) with a 95% confidence interval (CI). A random effects model or a fixed-effects model was used, depending on the heterogeneity of the studies. A total of 11 studies were included, comprising 650 OSA patients. The pooled results showed that CPAP therapy significantly decreased ICAM-1 (SMD = - 0.283, 95% CI - 0.464 to - 0.101, p = 0.002) and E-selectin levels (SMD = - 0.349, 95% CI - 0.566 to - 0.133, p = 0.002). In contrast, there was no significant improvement of VCAM-1 levels after CPAP treatment (SMD = - 0.160, 95% CI - 0.641 to 0.320, p = 0.513). Our meta-analysis demonstrated that CPAP treatment significantly decreased the circulating levels of ICAM-1 and E-selectin in OSA patients. Thus, ICAM-1 and E-selectin may be effective markers to evaluate CPAP therapy for reducing OSA cardiovascular risk in clinical practice.

Elevated Serum Levels of Progranulin and Soluble Vascular Cell Adhesion Molecule-1 in Patients with COVID-19.

BackgroundSevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is associated with the angiocentric inflammation and angiogenesis, yet the molecules involved in this process remain to be determined.MethodsWe did a cross-sectional study of a cohort of patients with COVID-19 in Zunyi, China between February 1 and March 30, 2020. Serum concentrations of PGRN were determined by enzyme-linked immunosorbent assay in patients with COVID-19 at hospital admission and at discharge. In parallel, the serum levels of soluble adhesion molecules, vascular cell adhesion molecule-1 (sVCAM-1), intercellular adhesion molecule-1 (sICAM-1), P-selectin (sP-selectin), and E-selectin (sE-selectin) were assayed by a human adhesion molecule multiplex kit. The association between serum PGRN levels and other laboratory test results was analyzed by Spearman correlation analysis.ResultsAt baseline, the median serum PGRN levels in patients with COVID-19 were 94.8 ng/mL [interquartile range (IQR): 66.6–119.6 ng/mL], which was significantly elevated compared with those in healthy controls (46.3 ng/mL, IQR: 41.8–55.6 ng/mL). Moreover, the median serum sVCAM-1 levels were significantly higher in COVID-19 patients (1396.0 ng/mL, IQR: 1019.1–1774.8 ng/mL) than those in healthy controls (612.4 ng/mL, IQR: 466.4–689.3 ng/mL). However, the levels of sICAM-1, sP-selectin, and sE-selectin were not significantly elevated in patients with COVID-19 when compared to healthy controls. Further analysis showed that serum PGRN levels were significantly positively associated with sVCAM-1 (r= 0.675, P= 0.008) and inversely with sICAM-1 (r= −0.609, P= 0.021) and aspartate aminotransferase levels (r= −0.560, P= 0.037) in patients with COVID-19 at hospital admission. In COVID-19 patients, serum PGRN and sVCAM-1 levels fell significantly after successful treatment.ConclusionThe present study demonstrates elevated serum PGRN and sVCAM-1 levels in patients with COVID-19, which may provide clues as to the mechanisms underlying the pathogenesis of COVID-19. Further studies are warranted to evaluate the potential of PGRN and sVCAM-1 as biomarkers and investigate their role in the pathogenesis of COVID-19.

Soluble vascular cell adhesion molecule-1 in patients with non-valvular atrial fibrillation

Background: Disturbances in atrial microcirculation is recognized as a risk factor for atrial fibrillation (AF). Aim: The aim of this study was to determine the associations between circulating soluble vascular cell adhesion molecule-1 (sVCAM-1) and the risk of AF and a one-year prognosis among consecutive inpatients. Methods: Eighty consecutive inpatients hospitalized due to non-valvular AF and 80 consecutive inpatients admitted for exacerbation of chronic coronary syndrome (control group) were enrolled in the study. A cardiologic workup was performed and blood sVCAM-1 concentration was determined using the ELISA method. Results: Patients with AF had similar blood sVCAM-1 concentration compared to the control group. AF patients treated with new oral anticoagulants (NOACs) were significantly less likely to have a sVCAM-1 concentration elevated above the median value than patients treated with warfarin (34.2% vs 65.8%; p = 0.01). Patients with an increased percentage of fat mass (FM) had lower sVCAM-1 concentration. The risk of all-cause mortality and MACE during follow-up rose in individuals with elevated sVCAM-1 (≥ 1242 and ≥ 587 ng/ml, respectively) with (OR; 95%CI): 5.39; 1.57-18.45; p = 0.007, and 6.00; 1.18-30.37; p = 0.03, respectively. Risk of death rose with increase in the ratio of sVCAM-1 and FM (1.02; 1.00-1.04; p = 0.019). Conclusions: Elevated sVCAM-1 was associated with all-cause mortality and MACE during one-year follow- up, but do not links the risk of AF. Use of NOACs may favorable affect endothelial function, A lower level of sVCAM-1 in obese patients may mediate the phenomenon of the “obesity paradox” in patients with AF.

Serum levels of cell adhesion molecules in patients with neuromyelitis optica spectrum disorder.

ObjectivesBlood–brain barrier (BBB) disruption is a critical pathological process involved in neuromyelitis optica spectrum disorder (NMOSD). Here, we characterized the profile of five cell adhesion molecules in patients with NMOSD.MethodsWe measured levels of cell adhesion molecules, including ICAM‐1, ICAM‐2, VCAM‐1, PECAM‐1, and NCAM‐1, in the serum of 28 patients with NMOSD, 24 patients with multiple sclerosis (MS), and 25 healthy controls (HCs).ResultsICAM‐2 levels (median: 394.8 ng/mL) were increased in patients with NMOSD compared with MS (267.1 ng/mL, P = 0.005) and HCs (257.4 ng/mL, P = 0.007), and VCAM‐1 and ICAM‐1 levels were higher in patients with NMOSD (641.9 ng/mL and 212.7 ng/mL, respectively) compared with HCs (465 ng/mL [P = 0.013] and 141.8 ng/mL [P = 0.002], respectively). However, serum PECAM‐1 levels were lower in patients with NMOSD (89.62 ng/mL) compared with MS (106.9 ng/mL, P = 0.015) and HCs (107.2 ng/mL, P = 0.007). Receiver operating characteristic curve analysis revealed that PECAM‐1 (area under the curve (AUC): 0.729) and ICAM‐2 (AUC: 0.747) had adequate abilities to distinguish NMOSD from MS, and VCAM‐1 (AUC: 0.719), PECAM‐1 (area under the curve: 0.743), ICAM‐1 (AUC: 0.778), and ICAM‐2 (AUC: 0.749) exhibited potential to differentiate NMOSD and HCs. Serum levels of PECAM‐1 also demonstrated a negative correlation with Kurtzke Expanded Disability Status Scale scores in patients with NMOSD.InterpretationOur results reveal possible BBB breakdown signals specifically observed in NMOSD and highlight the potential role of cell adhesion molecules as biomarkers of this disease.

The effect of intramuscular megadose of vitamin D injections on E-selectin, CRP and biochemical parameters in vitamin D-deficient patients with type-2 diabetes mellitus: A randomized controlled trial

Background and aimsInflammatory processes has been shown to be associated with the development of type 2 diabetes mellitus (T2DM) in which vitamin D supplementation might exert beneficial outcomes. We examined the effects of vitamin D supplement on inflammatory and cell adhesion molecule in patients with T2DM. MethodsThis study consisted of 50 patients with T2DM who had vitamin D deficiency. Participants were randomized into two groups of 25 in which the intervention group received two intramuscular injections of a 200000-IU vitamin D supplement, one at week 0 and another at week 4. The concentrations of fasting blood glucose (FBG), lipid profiles, liver enzymes, E-selectin, C-reactive protein (CRP), calcium, phosphorus, serum 25-hydroxyvitamin D [25(OH)D] and anthropometric indices were obtained before and after 8 weeks. ResultsVitamin D resulted in significant reductions in CRP(P = 0.01) and gamma glutamyl transferase (GGT) levels(P = 0.03) and significant increases in 25(OH)D concentrations(P = 0.01) in the intervention group compared with the control. Within-group comparisons showed that FBG decreased significantly in the intervention group(P = 0.04). No significant changes were observed regarding within- and between-group comparisons of the other markers. ConclusionVitamin D had beneficial effects on the levels of CRP, serum 25(OH)D and GGT among vitamin D deficient patients with T2DM. (http://www.irct.ir: IRCT2017100336539N1).

The Diagnostic Value of Serum L1CAM in Patients With Colorectal Cancer.

Objective:Colorectal cancer is one of the most important malignant cancer in the world with high incidence and mortality. Some studies have found that the expression of low serum L1 cell adhesion molecule is associated with poor prognosis in some malignancies. It is suggested that L1 cell adhesion molecule is a candidate serum marker for certain tumors. However, the relationship between serum L1 cell adhesion molecule and colorectal cancer, especially about the diagnostic value, is rarely reported. Therefore, this study aimed to evaluate the diagnostic potential of serum L1 cell adhesion molecule in patients with colorectal cancer.Methods:Enzyme-linked immunosorbent assay was carried out to detect L1 cell adhesion molecule level in sera of 229 patients with colorectal cancer and 145 normal controls. Receiver operating characteristic curves were employed to calculate the accuracy of diagnosis.Results:The levels of serum L1 cell adhesion molecule in the colorectal cancer group were significantly lower than that in normal controls (P < .05). In the normal group, the area under the receiver operating characteristic curve (area under the curve) of all colorectal cancer was 0.781 (95% confidence interval: 0.734-0.828) and early-stage colorectal cancer was 0.764 (95% confidence interval: 0.705-0.823). With optimized cutoff of 17.760 ng/mL, L1 cell adhesion molecule showed certain diagnostic value with specificity of 90.3% and sensitivities of 43.2% and 36.2% in colorectal cancer and early-stage colorectal cancer, respectively. Clinical data analysis showed that the levels of L1 cell adhesion molecule were significantly correlated with gender (P < .05) and early and late stages (P < .05). Furthermore, when compared with carcinoembryonic antigen, serum L1 cell adhesion molecule had significantly improved diagnostic accuracy for both colorectal cancer and early-stage colorectal cancer.Conclusions:Our study demonstrated that serum L1 cell adhesion molecule might be served as a potential biomarker for the diagnosis of colorectal cancer.

Influence of treatments on cell adhesion molecules in patients with systemic lupus erythematosus and rheumatoid arthritis: a review

Systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA) are autoimmune diseases characterized by changes in cell adhesion molecules (CAMs). To review the influence of the main drugs used in the treatment of SLE and RA on CAM levels. A bibliographic search was performed using electronic databases. The research included human studies, in vivo or in vitro, with an experimental or observational design, and with no limit of publication date or number of subjects. Animal studies and non-standard treatments were not considered. We included 21 studies, 3 on SLE and 18 on RA with monotherapy or combined trials. The most used drugs were cyclophosphamide (CY, in 2 studies) and methylprednisolone pulse (pMP, n = 2) in SLE; and methotrexate (MTX, n = 9) and infliximab (IFX, n = 4) in RA. In addition, the most frequently examined CAMs to predict response to treatment were vascular cell adhesion molecule-1 (VCAM-1, n = 2) in SLE, and intercellular adhesion molecule-1 (ICAM-1, n = 12), VCAM-1 (n = 12), and E-selectin (n = 14) in RA. After treatment, CAM levels were decreased in SLE and RA patients with active disease. It is concluded that the CAM biomarkers may reflect disease activity and the response to treatment in SLE and RA patients.

Effects of sitagliptin therapy on markers of low-grade inflammation and cell adhesion molecules in patients with type 2 diabetes

Inflammation and endothelial dysfunction are increasingly being recognized as key etiological factors in the development of atherosclerosis and subsequent cardiovascular disease. These pro-atherogenic factors are strongly correlated and are often found to co-segregate in patients with type 2 diabetes. The impact of sitagliptin, a selective inhibitor of dipeptidyl peptidase-4, on inflammation and markers of endothelial function remains to be fully characterized. ObjectiveThe objective of the present study was to examine the effects of treatment with sitagliptin on the plasma levels of various markers of low-grade inflammation and cell adhesion molecules in patients with type 2 diabetes. Methods and resultsThirty-six subjects with type 2 diabetes (30 men/6 postmenopausal women with a mean age of 58.1±6.4years and a body mass index of 30.7±4.9kg/m2) were recruited into this double-blind, cross-over study using sitagliptin (100mg/d) or placebo, each for a 6-week period, including a 4-week washout period between the two phases. Blood samples were taken at the end of each phase of treatment. Compared with placebo, treatment with sitagliptin significantly reduced the plasma levels of C-reactive protein (CRP) (44.9%, P=0.006), interleukin (IL)-6 (24.7%, P=0.04), IL-18 (7.3%, P=0.004), secreted phospholipase-A2 (sPLA2) (12.9%, P=0.04), soluble intercellular adhesion molecule-1 (5.3%, P=0.002), and E-selectin (5.9%, P=0.005). A significant inverse correlation was found between changes in glucagon-like peptide-1 (GLP-1) and changes in CRP levels (r=0.41, P=0.01) following sitagliptin therapy. Sitagliptin therapy had more pronounced effects in subjects with higher levels of inflammatory markers and cell adhesion molecules compared with subjects with lower levels. ConclusionsTreatment with sitagliptin for 6weeks reduced plasma markers of low-grade inflammation and cell adhesion molecules, most likely by increasing plasma GLP-1 levels and improving glucose-insulin homeostasis. These beneficial effects of sitagliptin might represent a further advantage in the management of diabetes and its proatherogenic comorbidities.

SVCAM-1 vascular cell adhesion molecules and heart structural and functional changes in patients with acute left ventricular aneurism following myocardial infarction

Aim. To study the expression of sVCAM-1 soluble vascular cell adhesion molecules in patients with acute left ventricular aneurysm following myocardial infarction and assess the relationship with the processes of heart remodeling. Methods. 170 patients diagnosed with acute myocardial infarction in the presence of Q-wave were examined. The expression of sVCAM-1 soluble vascular cell adhesion molecule, electrocardiogram and Doppler echocardiography changes were studied depending on comorbidities and the development of acute left ventricular aneurysm following myocardial infarction. Results. ST-segment elevation was still detectable in patients with left ventricular aneurysm compared to patients with no aneurism on the 3rd and 5th day after the disease onset, its amplitude was significantly higher, no dynamic changes of the T-wave in the anterior chest leads were registered. The prevalence of left ventricular dilatation, mitral regurgitation, reduced systolic function of left ventricle and type II diastolic dysfunction was higher in patients with left ventricular aneurysm. The relationship between sVCAM-1 vascular adhesion molecules expression with early remodeling after the myocardial infarction and left ventricular aneurysm development in acute stage of myocardial infarction in the presence of Q-wave was revealed. Conclusion. In the presence of such comorbidities as hypertension and diabetes, a higher level of sVCAM-1 vascular adhesion molecules expression was revealed in patients with left ventricular aneurysm following myocardial infarction. ST-segment elevation and no dynamic changes of the T-wave were still registered by electrocardiography till the 5th day after the disease onset. Amplitudes of ST-segment and T-wave were significantly higher in patients with left ventricular aneurysm following myocardial infarction compared to patients with no complications of myocardial infarction.

Serum level of soluble vascular cell adhesion molecule in patients with hepatocellular carcinoma and its association with severity of liver disease

Background. VCAM-1 (soluble vascular cell adhesion molecule-1) plays a role in liver angiogenesis. Hepatocellular carcinoma (HCC) has important angiogenic activity, so expression of VCAM-1 may be pathogenic. Aim. To assess the association between serum VCAM-1 (sVCAM-1) levels and features of tumour and liver disease in patients with and without HCC, and to study the influence of HCC treatment on sVCAM-1 levels.Material and methods. Concentrations in peripheral (sVCAM-1-P) and hepatic (sVCAM-1-H) veins were analysed using ELISA in 134 consecutive patients with chronic liver disease between May 2004 and February 2006, who underwent a splanchnic haemodynamic study. Of these patients, 58 had HCC.Results. sVCAM-1-P and sVCAM-1-H were well correlated in both groups. No association was found between sVCAM-1-H and tumour features. No differences were observed in sVCAM-1-H between HCC and non-HCC cirrhotic patients. There was a significant linear association between Child-Pugh stage and sVCAM-1-H in HCC-patients (Child-Pugh A [2,485 ± 1,294 ng/mL] vs. Child-Pugh B [3,408 ± 1,338 ng/mL] vs. Child-Pugh C [4,096 ± 862 ng/ mL]; p = 0.007). Seven non-cirrhotic HCC patients had a significantly lower sVCAM-1-H than cirrhotic HCC patients. Treatment of HCC leads to an increase in sVCAM-1-H levels although this was not associated with the necrosis response to treatment.Conclusions. sVCAM-1 levels are more closely associated with the severity of underlying liver disease than with the presence of HCC. sVCAM-1 levels are not associated with tumour features or invasiveness; therefore, sVCAM-1 does not seem to play an important role in the angiogenic processes of HCC.

Higher serum levels of soluble intracellular cell adhesion molecule‐1 and soluble vascular cell adhesion molecule predict peripheral artery disease in haemodialysis patients

Serum levels of soluble intracellular cell adhesion molecule-1 (sICAM-1), soluble vascular cell adhesion molecule-1 (sVCAM) and monocyte chemotactic protein 1 (MCP-1), are elevated in patients with peripheral artery disease (PAD). However, the levels of these cell adhesion molecules in patients undergoing haemodialysis (HD) are unclear. A total of 112 HD patients were included and PAD was diagnosed using the ankle-brachial index and Doppler ultrasound. Serum levels of sICAM-1, sVCAM-1 and MCP-1 were assayed using enzyme linked immunosorbent assay. Out of 106 HD patients, 31 (27.7%) were diagnosed with PAD. After adjusting for risk factors, higher serum levels of sVCAM-1 and sICAM-1 were associated with PAD in HD patients, with an odds ratio of 5.3 (95% CI 3.3-65.5) and 2.7 (95% CI 1.2-21.8) respectively. Using sVCAM-1 and sICAM-1 for diagnosis of PAD in HD patients, sVCAM-1 had a sensitivity of 72.4% and specificity of 62.3% for sVCAM-1 and sICAM-1 had a sensitivity of 89.3% and a specificity of 40%. MCP-1 was not associated with PAD in HD patients. In addition, the fistula of HD patients with PAD had a lower A-V access flow. sVCAM-1 and sICAM-1 was associated with higher risk of PAD in HD patients. Moreover, HD patients with PAD had a lower blood flow and lower A-V access flow. Our results showed that sVCAM-1 and sICAM-1 may be used as screening markers for PAD in HD patients.

Effects of short-term therapy with glibenclamide and repaglinide on incretin hormones and oxidative damage associated with postprandial hyperglycaemia in people with type 2 diabetes mellitus

Aim To examine the effects of glibenclamide and repaglinide on glucose stimulated insulin release, incretins, oxidative stress and cell adhesion molecules in patients with type 2 diabetes suboptimally treated with metformin. Methods A randomized clinical trial was performed recruiting 27 subjects (HbA 1c between 7.5 and 10.5%) free from cardiovascular and renal disease. Glucose, insulin, C-peptide, glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic peptide (GIP), total antioxidant status, F 2-isoprostane, interleukin-6 and cell adhesion molecules were measured during an oral glucose load at baseline and after eight weeks of treatment. The areas under the curve were analysed at 45, 60 and 120 min (AUC 45, AUC 60, AUC 120). Results Significant improvements in glucose were observed with repaglinide (HBA 1c: −1.5%, fasting glucose: −2.8 mmol/L, 2-h glucose: −3.7 mmol/L, AUC 120: −18.9%) and glibenclamide (−1.0%, −2.2 mmol/L, −2.5 mmol/L, −17.5%). Repaglinide was also associated with an increase in the AUC 60 and AUC 120 for insulin (+56%, +61%) and C-peptide (+41%, +36%). GLP-1, GIP, IL-6, ICAM-1 and E-selectin levels did not change in either group. No association was observed between GLP-1, GIP-1 and plasma markers of oxidative stress. Conclusion Repaglinide is associated with improved postprandial glycaemic control via insulin and C-peptide release. We observed no direct effects of glibenclamide or repaglinide on plasma levels of GLP-1 or GIP. We observed no associations of GLP-1 and GIP with plasma markers of oxidative stress.

Anti-C1q antibodies have higher correlation with flares of lupus nephritis than other serum markers

Autoantibodies are important in the diagnosis and classification of systemic lupus erythematosus (SLE), but whether they correlate with changes in disease activity within individual patients is controversial. We assessed the association between changes in SLE global and renal activity and changes in several autoantibodies and cell adhesion molecules in patients with SLE. Stored sera collected at two or three clinic visits from each of 49 SLE patients (91% female, 59% African-American, 31% Caucasian, 10% other ethnicity, 38% under 30 years, 41% between 30-44 years, and 21% 45-63 years) were analyzed. The visits were chosen to include one visit with proteinuria, and one or two without, for each patient. Global disease activity was measured by the Physician's Global Assessment (PGA), SELENA-SLEDAI (SLE Disease Activity Index modified to exclude anti-dsDNA and complement) and renal activity assessed by urine protein (by urine dipstick) and Renal Activity Score. Sera were assayed for anti-C1q, anti-chromatin, anti-dsDNA, anti-ribosomal P, monocyte chemotactic protein-1 (MCP-1), vascular cell adhesion molecule (VCAM) intercellular adhesion molecule (ICAM) and complement. The associations between changes in disease activity and changes in biomarker levels were assessed. In terms of global disease activity, anti-C1q had the highest association with the PGA (p = 0.09) and was strongly associated with modified SELENA-SLEDAI (p = 0.009). In terms of renal activity, anti-C1q had the highest association with proteinuria (p = 0.079), and was strongly associated with Renal Activity Score (p = 0.006). Anti-C1q performed the best of the potential biomarkers, being significantly associated with the modified SELENA-SLEDAI and with the Renal Activity Score. This study indicates the potential superior utility of anti-C1q over anti-dsDNA and other measures to track renal activity.

Análisis comparativo de la expresión de moléculas de adhesión celular en linfomas cutáneos (micosis fungoide/síndrome de Sézary) y dermatosis inflamatorias mediadas por células T

Introduction Cell adhesion molecules play a pivotal role in the establishment of T-cell populations in the skin. In this study, we quantify the expression of cell adhesion molecules in patients with cutaneous T-cell lymphoma (CTCL) and compare it with the expression found in other skin diseases. Material and methods Frozen material was obtained from 42 patients in 5 different groups: early CTCL, comprising patients with patch- and plaque-stage of mycosis fungoides ( n=11); advanced CTCL ( n=7), comprising patients with mycosis fungoides ( n=3) and Sézary syndrome ( n=4); inflammatory skin disease ( n=12), comprising patients with psoriasis ( n=9) and atopic dermatitis ( n=3); chronic skin diseases with persistent plaques that do not fulfil the histological criteria for mycosis fungoides (pre-CTCL) ( n=8); and healthy volunteers ( n=4). Expression of the following cell adhesion molecules was analyzed: lymphocyte function-associated antigen 1, intercellular adhesion molecule 1 (ICAM-1), ICAM-3, cutaneous lymphocyte-associated antigen, E-selectin, very late antigen 4, vascular cell adhesion molecule 1, alphaEbeta7 integrin, and E-cadherin. Results The immunohistochemical analyses used here revealed statistically significant differences between CTCL and other skin diseases but not between early and advanced CTCL. The expression of alphaEbeta7 integrin and ICAM-3 in the epidermis per high-power field (400× magnification) allowed the different groups to be distinguished from each other, except for advanced CTCL and pre-CTCL. There were statistically significant differences between advanced CTCL and pre-CTCL in terms of the expression of E-selectin at 400× magnification and the expression of ICAM-1 in a honeycomb pattern in epidermal keratinocytes. Conclusions The expression of cell adhesion molecules involved in the adhesion and migration of lymphocytes in the skin does not differ significantly between initial and advanced stages of CTCL.

CNS Elevation of Vascular and Not Mucosal Addressin Cell Adhesion Molecules in Patients with Multiple Sclerosis

The mucosal addressin cell adhesion molecule (MAdCAM) and vascular cell adhesion molecule (VCAM) appear to play roles in the recruitment of leukocytes to specialized endothelium lining the gastrointestinal tract. The purpose of this study was to clarify the role of MAdCAM and VCAM in the central nervous system by comparing protein expression in patients with multiple sclerosis (MS) and control subjects by immunohistochemistry. Specific antibodies to human VCAM and MAdCAM were used to confirm expression in control and MS nervous system specimens by immunohistochemistry. VCAM immunoreactivity was detected in endothelial cells, perivascular tissue, and in some cases, leukocytes within the meninges, gray, and white matter, of both controls and MS patients. VCAM immunoreactivity was maximal in a patient with acute active plaques, but of lower intensity and reduced distribution in controls and those with chronic active or inactive MS plaques. In contrast, MAdCAM immunoreactivity could not be detected in brain tissue from unaffected or MS patients. Taken together, these data support a role of VCAM, but not MAdCAM in the development of MS.

Comparative Analysis of the Expression of Cell Adhesion Molecules in Cutaneous T-Cell Lymphomas (Mycosis Fungoides/Sézary Syndrome) and Inflammatory Skin Diseases

Introduction Cell adhesion molecules play a pivotal role in the establishment of T-cell populations in the skin. In this study, we quantify the expression of cell adhesion molecules in patients with cutaneous T-cell lymphoma (CTCL) and compare it with the expression found in other skin diseases. Material and methods Frozen material was obtained from 42 patients in 5 different groups: early CTCL, comprising patients with patch- and plaque-stage mycosis fungoides (n=11); advanced CTCL (n=7), comprising patients with mycosis fungoides (n=3) and Sézary syndrome (n=4); inflammatory skin disease (n=12), comprising patients with psoriasis (n=9) and atopic dermatitis (n=3); chronic skin diseases with persistent plaques that do not fulfil the histological criteria for mycosis fungoides (pre-CTCL) (n=8); and healthy volunteers (n=4). Expression of the following cell adhesion molecules was analyzed: lymphocyte function-associated antigen 1, intercellular adhesion molecule 1 (ICAM-1), ICAM-3, cutaneous lymphocyte-associated antigen, E-selectin, very late antigen 4, vascular cell adhesion molecule 1, αEβ7 integrin, and E-cadherin. Results The immunohistochemical analyses used here revealed statistically significant differences between CTCL and other skin diseases but not between early and advanced CTCL. The expression of αEβ7 integrin and ICAM-3 in the epidermis per high-power field (400× magnification) allowed the different groups to be distinguished from each other, except for advanced CTCL and pre-CTCL. There were statistically significant differences between advanced CTCL and pre-CTCL in terms of the expression of E-selectin at 400× magnification and the expression of ICAM-1 in a honeycomb pattern in epidermal keratinocytes. Conclusions The expression of cell adhesion molecules involved in the adhesion and migration of lymphocytes in the skin does not differ significantly between initial and advanced stages of CTCL.

Enhanced mobilization of CD34+ progenitor cells expressing cell adhesion molecules in patients with STEMI

Adult stem cells can contribute to myocardial regeneration after ischemic injury. The aim of the study was to determine (1) the amount of mobilized CD34(+)/CD117(+), CD34(+)/KDR(+) cells into peripheral blood (PB) in relation to inflammatory and haematopoietic cytokines, (2) the presence of circulating CD34(+) cells, expressing cell adhesion molecules (CAM), in patients with ST-segment elevation myocardial infarction (STEMI) in comparison to patients with coronary artery disease (CAD). Twenty-three patients with STEMI (<12 h), 24 patients with CAD and 15 control subjects were enrolled in this study. The patients were matched in age, 2-CAD, ejection fraction (45%) and end-diastolic volume index (70 ml/m(2)). The number of stem cells and the expression of adhesion molecules were quantified by use of flow cytometry. Inflammatory cytokines [interleukin-6 (IL-6), granulocyte colony-stimulating factor (G-CSF), vascular endothelial growth factor] and chemotactic factors as stromal cell-derived factor-1 (SDF-1), hepatocyte growth factor (HGF) were determined by ELISA. The amount of circulating progenitor cells including CD34(+)/CD117(+) and CD34(+)/KDR(+) cells was significantly higher in patients with STEMI than in patients with CAD (CD34(+)/CD117(+) 433 +/- 128 vs. 100 +/- 17, P = 0.012; CD34(+)/KDR(+) 253 +/- 41 vs. 128 +/- 24, P = 0.02). The mobilization of CD34(+) progenitor cells expressing CXCR4-receptor, lymphocyte function-associated antigen-1 (LFA-1), very late antigen-4 (VLA-4) and ICAM-1 into PB was significantly higher in patients with STEMI compared to CAD (CD34(+)/CXCR4(+) 740 +/- 327 vs. 136 +/- 23, P = 0.006; CD34(+)/LFA-1 976 +/- 227 vs. 329 +/- 41, P = 0.025; CD34(+)/VLA4(+) 830 +/- 161 vs. 330 +/- 31, P = 0.007; CD34(+)/ICAM(+) 387 +/- 66 vs. 144 +/- 26, P < 0.001). Additionally, the cytokines G-CFS, IL-6 and HGF were upregulated and significantly increase in the STEMI group compared with controls and CAD (G-CSF 50.6 +/- 6.8 vs. 23 +/- 3 vs. 23.8 +/- 2, P (Co vs. STEMI) < 0.001, P (Co vs. CAD) = n.s., P (STEMI vs. CAD) < 0.001; IL-6 8.4 +/- 0.6 vs. 3.8 +/- 1.9 vs. 2.6 +/- 1, P (Co vs. STEMI) < 0.001, P (Co vs. CAD) = n.s., P (STEMI vs. CAD) < 0.001; HGF 4,502 +/- 461 vs. 686 +/- 195 vs. 1,746 +/- 461, P (Co vs. STEMI) < 0.001, P (Co vs. CAD) = n.s., P (STEMI vs. CAD) < 0.001), while the level of SDF-1 was increased in patients with CAD compared to controls and patients with STEMI (3,035 +/- 286 vs. 2,028 +/- 76 vs. 2,154 +/- 234, P (Co vs. STEMI) = n.s., P (Co vs. CAD) = n.s., P (STEMI vs. CAD) = 0.005). The study demonstrates in patients with STEMI an increased mobilization of progenitor cells like CD34(+)/CD117(+) and CD34(+)/KDR(+) compared to CAD. Furthermore, we could shown that in patients with STEMI the mobilization of CD34(+) progenitor cells with expressed CAM was increased. It is to speculate that an enhanced expression of adhesion molecules may increase the transmigration and implantation of progenitor cells into ischemic myocardium for myocardial repair.

RETRACTED ARTICLE: Evaluation of renal vascular lesions using thrombomodulin and vascular cell adhesion molecule-1 in patients with biopsy-proven lupus nephritis.

The authors discovered post-publication that the data submitted was incorrect. According to the study data, the patients were all IV lupus nephritis patients. However, on further review, the authors found that some patients in the study were not IV lupus nephritis, which meant that the diagnosis was wrong and the clinical data and the levels of thrombomodulin and vascular cell adhesion molecule-1 were not correctly reported. The authors apologize for this error, and have requested the manuscript to be withdrawn. Clin Rheumatol DOI 10.1007/s10067-009-1167-2

Elevation of Activated Platelet-Dependent Chemokines and Soluble Cell Adhesion Molecules in Patients with Hematologic Malignancies and High Levels of β-D-Glucan

Most invasive fungal infections such as candidemia are frequent in patients with hematologic malignancies. We measured cytokines/chemokines (IL-6, IL-8, monocytic chemoattractant protein 1, RANTES and epithelial neutrophil-activating peptide 78), soluble molecules (sFas, sE-selectin and soluble vascular cell adhesion molecule 1) and platelet activation markers (soluble CD40 ligand, sP-selectin and platelet-derived microparticles) in patients with hematologic malignancies under prophylactic treatment with an antifungal drug (fosfluconazole). We classified patients into 2 groups by the level of β-D-glucan. The level of C-reactive protein was higher in the high β-D-glucan group (>5 pg/ml) than in the low β-D-glucan group. However, there were no differences in the levels of other parameters (peripheral blood cells, glutamic-oxaloacetic transaminase, glutamic-pyruvic transaminase, lactate dehydrogenase, blood urea nitrogen and creatinine). Patients in the high β-D-glucan group exhibited a significant elevation of several chemokines, soluble molecules and platelet activation markers compared with those in the low β-D-glucan group, but the levels of IL-8, monocytic chemoattractant protein 1 and sFas did not differ significantly. The levels of C-reactive protein and IL-6 increased significantly after 1 or 2 weeks on fosfluconazole in both groups. In contrast, the high β-D-glucan group exhibited a significant decrease in chemokines, soluble markers and platelet-derived microparticles compared with the low β-D-glucan group after treatment with fosfluconazole, although the patients in the low β-D-glucan group exhibited no significant changes. Furthermore, the levels of RANTES, epithelial neutrophil-activating peptide 78, soluble vascular cell adhesion molecule 1 and sE-selectin correlated positively with platelet-derived microparticles in the high β-D-glucan group. These findings suggest that fungal infection may modulate the vascular events in which some platelet-related chemokines are involved.

Relationship of transforming growth factor‐beta1 with tumour necrosis factor‐alpha and endothelial activation in patients with stable renal transplantation

To evaluate whether or not transforming growth factor-beta(1) is related to inflammation markers and to intercellular and vascular cell adhesion molecules in patients with stable renal transplantation. Serum concentrations of transforming growth factor-beta(1), tumour necrosis factor-alpha, C-reactive protein and adhesion molecules were analysed in 33 renal transplanted patients, 33 patients with chronic renal insufficiency (matched to the transplanted group for level of renal function), and 33 hypertensives with normal renal function. anova, Student's t-test and simple regression analysis were used to analyse the data. Transplanted patients showed higher values than hypertensives of transforming growth factor-beta(1), tumour necrosis factor-alpha, C-reactive protein and adhesion molecules (P < 0.0001 for all). Renal insufficiency group exhibited higher concentrations of transforming growth factor-beta(1), tumour necrosis factor-alpha, C-reactive protein and adhesion molecules than hypertensives (P < 0.0001 for all). Transplanted and renal insufficiency patients had similar blood pressure and renal function levels, and transforming growth factor-beta(1), tumour necrosis factor-alpha, C-reactive protein and adhesion molecules were not significantly different. In transplanted and in renal insufficiency groups transforming growth factor-beta(1), adhesion molecules and tumour necrosis factor-alpha correlated significantly each other and with glomerular filtration rate (P < 0.001 for all). In long-term renal transplantation inflammation and endothelial activation biomarkers, the pro-fibrotic cytokine transforming growth factor-beta(1) and kidney function are interrelated. Because of the relevant role that inflammation, organ fibrosis and graft dysfunction may play against renal and cardiovascular survival of graft recipients, a better comprehension of the interactions between these variables is needed.