VCAM-1, ICAM-1, and E-Selectin in IgA Nephropathy and Schönlein-Henoch Syndrome: Differences between Tissue Expression and Serum Concentration

Mrowka, Christian; Heintz, Bernhard; Sieberth, Heinz–Günter

doi:10.1159/000045290

Cited by 29 publications

(20 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In addition, the expression of ICAM-1 is induced on the proximal tubule epithelium associated with glomerular [18]and interstitial cellular infiltration seen by light microscopy [13]and characterized by monoclonal antibodies directed to leukocytes [20, 26]. The serum ICAM-1 levels in histologically severe forms [27]and in both exacerbating clinical episodes and during quiescence [26, 28]are similar to those in healthy controls. Thus, the abnormal expression of ICAM-1 on the tubular epithelium appears to be a specific local phenomenon rather than a reflection of the serum level, but its significance is uncertain.…”

Section: Discussionmentioning

confidence: 99%

Tubular and Interstitial Expression of ICAM-1 as a Marker of Renal Injury in IgA Nephropathy

Arrizabalaga¹,

Solé

Abellana

et al. 2003

Am J Nephrol

View full text Add to dashboard Cite

Background: The upregulated renal expression of intercellular adhesion molecule 1 (ICAM-1) is associated with glomerular and interstitial infiltration of leukocytes. Aim: To test the hypothesis that renal expression of ICAM-1 may be predictive in the highly variable IgA nephropathy (IgAN). Methods: ICAM-1 (CD54) in tubular epithelium and interstitial leukocytes, macrophages (CD14), and T cells (CD3) were assessed using avidin-biotin-peroxidase in renal biopsy specimens from 45 patients with IgAN and from 29 patients with no glomerulonephritis. Results: In IgAN, tubular ICAM-1+ was seen in 25 of 45 (55%) biopsy specimens, associated with glomerular hypercellularity, glomerulosclerosis involving less than 50% of the glomerular area, interstitial cellular infiltration, tubular atrophy, and proteinuria (U = 44, p = 0.005). Interstitial ICAM-1+ leukocytes were correlated with glomerulosclerosis involving less and more than 50% of the glomerular area, tubular atrophy, interstitial fibrosis, and serum creatinine concentration (r = 0.6343, p < 0.001). In patients with an increase of 50% in the serum creatinine concentration, interstitial ICAM-1+ leukocytes and CD14+ and CD3+ cells were significantly more numerous than in patients with a stable creatinine concentration. In patients with no glomerulonephritis, tubular ICAM-1+ was seen in 7 of 29 (24%) biopsy specimens, inversely correlated with the number of normal glomeruli and associated with glomerulosclerosis covering more than 50% of the glomerular area, tubular atrophy, and creatinine. Conclusions: Tubular and interstitial expression of ICAM-1 can be a marker of tubulointerstitial disturbance in IgAN. Interstitial ICAM-1 may be an adverse predictor of disease progression.

show abstract

Section: Discussionmentioning

confidence: 99%

Tubular and Interstitial Expression of ICAM-1 as a Marker of Renal Injury in IgA Nephropathy

Arrizabalaga¹,

Solé

Abellana

et al. 2003

Am J Nephrol

View full text Add to dashboard Cite

show abstract

“…One such molecule, VCAM-1, is expressed on the surface of endothelial cells and promotes the binding and movement of lymphocytes and eosinophils across vascular endothelium (1)(2)(3). VCAM-1-mediated leukocyte recruitment and migration are implicated in the pathogenesis of several disease states, including inflammatory bowel disease (4), conjunctivitis (5), nephropathy (6,7), and arthritis (8). The essential role of VCAM-1 in tissue injury has been corroborated in a number of animal models.…”

mentioning

confidence: 99%

Unconjugated Bilirubin Inhibits VCAM-1-Mediated Transendothelial Leukocyte Migration

Keshavan

Deem²,

Schwemberger

et al. 2005

The Journal of Immunology

145

View full text Add to dashboard Cite

During lymphocyte migration, engagement of VCAM-1 stimulates the generation of endothelial cell-derived reactive oxygen species (ROS) and activation of matrix metalloproteinases, facilitating endothelial retraction. Because bilirubin is a potent antioxidant, we examined the hypothesis that this bile pigment inhibits VCAM-1-dependent cellular events. The migration of isolated murine splenic lymphocytes across monolayers of murine endothelial cell lines (which constitutively express VCAM-1) is significantly inhibited by physiological concentrations of bilirubin, in the absence of an effect on lymphocyte adhesion. Bilirubin administration also suppresses VCAM-1-stimulated ROS generation and reduces endothelial cell matrix metalloproteinase activity. In a murine asthma model characterized by VCAM-1-dependent airway inflammation, treatment of C57BL6/J mice with i.p. bilirubin decreases the total leukocyte count in the lung parenchyma and lavage fluid, through specific inhibition of eosinophil and lymphocyte infiltration. Blood eosinophil counts were increased in bilirubin-treated animals, while VCAM-1 expression in the capillary endothelium and cytokine levels in both lung lavage and supernatants from cultured lymph node lymphocytes were unchanged, suggesting that bilirubin inhibits leukocyte migration. Conclusion: bilirubin blocks VCAM-1-dependent lymphocyte migration in vitro and ameliorates VCAM-1-mediated airway inflammation in vivo, apparently through the suppression of cellular ROS production. These findings support a potential role for bilirubin as an endogenous immunomodulatory agent.

show abstract

“…26,[29][30][31][32][33][34] In addition, elevated circulating VCAM-1 has been shown to be correlated with increased VCAM-1 expression from renal biopsy in IgA nephropathy. 35 E-selectin is also found to be a strong predictor of severely increased albuminuria and coronary artery disease in patients with type 1 diabetes. 36,37 In another study VCAM-1 and E-selectin showed positive associations with retinopathy, albuminuria, and CVD.…”

Section: Discussionmentioning

confidence: 94%

Albuminuria Is Associated with Elevated Acute Phase Reactants and Proinflammatory Markers in HIV-Infected Patients Receiving Suppressive Combination Antiretroviral Therapy

O-charoen

Ndhlovu

Gangcuangco

et al. 2014

AIDS Research and Human Retroviruses

View full text Add to dashboard Cite

Albuminuria among HIV-infected individuals has been found to be associated with cardiovascular disease (CVD) and mortality. Inflammation has been associated with albuminuria. The pathophysiology of albuminuria in HIV-infected individuals is poorly understood. We investigated the association of albuminuria with inflammatory biomarkers among HIV-infected individuals on combination antiretroviral therapy (cART). This is a cross-sectional analysis of participants enrolled in the Hawaii Aging with HIV-Cardiovascular Cohort. Plasma inflammatory biomarkers were assessed using the Milliplex Human Cardiovascular disease multiplex assays. A random urine sample was collected for albumin measurement. Albuminuria was defined as urine albumin-tocreatinine ratio of ‡ 30 mg/g. Framingham risk score was calculated and divided into three classes. Simple and multivariable logistic regression analyses were utilized to assess the correlation between plasma inflammatory biomarkers and albuminuria and were adjusted for Framingham risk category. Among 111 HIV-infected patients [median (IQR) age of 52 (46-57) years, 86% male, median (IQR) CD4 count of 489 (341-638) cells/ mm 3 , 85% with HIV RNA < 50 copies/ml], 18 subjects (16.2%) had moderately increased albuminuria (albuminuria range between 30 and 300 mg/g) and 2 subjects (1.8%) had severely increased albuminuria (albuminuria more than 300 mg/g). In multivariable logistic models, sE-selectin, sVCAM-1, CRP, SAA, and SAP remained significantly associated with albuminuria after adjustment of CVD risk factors. This study showed an association between inflammation and albuminuria independent of previously reported risk factors for albuminuria in HIV-infected subjects who were on combination antiretroviral therapy (cART). Chronic inflammation despite potent antiretroviral treatment may contribute to higher rates of albuminuria among HIVinfected patients.

show abstract

VCAM-1, ICAM-1, and E-Selectin in IgA Nephropathy and Schönlein-Henoch Syndrome: Differences between Tissue Expression and Serum Concentration

Cited by 29 publications

References 20 publications

Tubular and Interstitial Expression of ICAM-1 as a Marker of Renal Injury in IgA Nephropathy

Tubular and Interstitial Expression of ICAM-1 as a Marker of Renal Injury in IgA Nephropathy

Unconjugated Bilirubin Inhibits VCAM-1-Mediated Transendothelial Leukocyte Migration

Albuminuria Is Associated with Elevated Acute Phase Reactants and Proinflammatory Markers in HIV-Infected Patients Receiving Suppressive Combination Antiretroviral Therapy

Contact Info

Product

Resources

About