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Actin S-nitrosylation inhibits neutrophil beta2 integrin function.

Stephen R Thom¹, Veena M Bhopale, D Joshua Mancini

¹Institute for Environmental Medicine, Department of Emergency Medicine, University of Pennsylvania Medical Center, Philadelphia, Pennsylvania 19104-6068, USA.

The Journal of Biological Chemistry

|February 20, 2008

Summary

Hyperoxia, or high oxygen, inhibits neutrophil adhesion by altering actin cytoskeleton. This process involves reactive species and S-nitrosylation, leading to reduced beta(2) integrin function.

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Quantitative In vitro Assay to Measure Neutrophil Adhesion to Activated Primary Human Microvascular Endothelial Cells under Static Conditions

Quantitative In vitro Assay to Measure Neutrophil Adhesion to Activated Primary Human Microvascular Endothelial Cells under Static Conditions

Published on: August 23, 2013

Area of Science:

Cellular Biology
Immunology
Biochemistry

Background:

Neutrophil adhesion is critical for immune response.
Hyperoxia (high oxygen) can impair neutrophil function.
The precise mechanism of hyperoxia-induced neutrophil dysfunction is not fully understood.

Purpose of the Study:

To investigate the mechanism by which hyperoxia inhibits neutrophil beta(2) integrin adhesion.
To identify the molecular players involved in hyperoxia-induced changes in neutrophil adhesion.

Main Methods:

Exposure of neutrophils to hyperoxia.
Measurement of reactive species synthesis (nitric oxide synthase, myeloperoxidase).
Assessment of protein S-nitrosylation (beta-actin, profilin).
Analysis of actin polymerization and filament formation.
Evaluation of beta(2) integrin clustering and neutrophil adhesion.

Main Results:

Hyperoxia increased reactive species synthesis.
Excessive S-nitrosylation of beta-actin and profilin was observed.
S-nitrosylation of actin led to shorter actin filaments, altered polymerization, and inhibited beta(2) integrin clustering.
Reversal of S-nitrosylation or 'inside-out' activation restored neutrophil adhesion.

Conclusions:

Hyperoxia inhibits neutrophil beta(2) integrin-dependent adhesion through cytoskeletal alterations.
Reactive species and S-nitrosylation of actin are key mediators of this inhibition.
Understanding this mechanism may offer therapeutic targets for hyperoxia-induced lung injury.