Vitamin E protects against polymorphonuclear leukocyte-dependent adhesion to endothelial cells

Area of Science:

• Immunology
• Nutritional Science
• Biochemistry

Background:

• Polymorphonuclear leukocytes (PMN) express CD11b/CD18, a molecule crucial for cell adhesion.
• Activation of PMN by stimuli like fMLP and oxLDL increases CD11b/CD18 expression, promoting inflammation.
• Alpha-tocopherol (vitamin E) is an antioxidant with potential anti-inflammatory properties.

Purpose of the Study:

• To investigate the effect of alpha-tocopherol on CD11b/CD18 surface expression in PMN.
• To determine if alpha-tocopherol influences PMN adherence to endothelial cells.
• To explore the underlying molecular mechanisms, including protein kinase C (PKC) and protein kinase A (PKA) pathways.

Main Methods:

• PMN were stimulated with fMLP or oxLDL, with or without alpha-tocopherol pretreatment.
• CD11b/CD18 surface expression was measured using flow cytometry.
• PMN adherence to endothelial cells was assessed.
• PKC and PKA activity assays were performed.
• Studies included in vitro assays and analysis of PMN from adults supplemented with alpha-tocopherol.

Main Results:

• Alpha-tocopherol reduced CD11b/CD18 expression on PMN in a dose-dependent manner.
• Serum alpha-tocopherol levels in supplemented adults inversely correlated with PMN CD11b/CD18 expression.
• Alpha-tocopherol pretreatment decreased PMN adherence to endothelial cells.
• PKC activation was involved in CD11b/CD18 up-regulation, and alpha-tocopherol slightly inhibited this activation.

Conclusions:

• Alpha-tocopherol effectively reduces CD11b/CD18 expression and PMN adherence, suggesting an anti-inflammatory role.
• The mechanism may involve the modulation of PKC signaling pathways.
• Dietary vitamin E supplementation could be a strategy to mitigate inflammatory processes mediated by PMN.