[Frontiers in Bioscience 17, 2278-2283, June 1, 2012]

Neutrophils in acute lung injury

Xiaohong Zhou1, Qingchun Dai2, Xinli Huang1

1Department of Pathophysiology, Hebei Medical University, 326 Xinshinan Road, Shijiazhuang, 050091, China, 2Department of Emergency, Cangzhou Central Hospital, 201 Xinhuaxi Road, Cangzhou, 061001, China

TABLE OF CONTENTS

1. Abstract
2. Introduction
3. PMN attachment and recruitment
4. PMN adhesion
4.1. Selectins family
4.2. Immunoglobulin superfamily
4.3. Integrin family
5. PMN activation and emigration
6. PMN release damage mediators after stimulation
6.1. Oxygen free radicals
6.2. Neutrophil elastase (NE)
6.3. Cytokines
7. PMN apoptosis
8. Conclusion
9. Acknowledgements
10. References

1. ABSTRACT

Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) are characterized by lung edema due to increased permeability of the alveolar-capillary barrier and subsequent impairment of arterial oxygenation. Lung edema, and endothelial and epithelial injury are accompanied by an influx of neutrophils into the interstitium and alveolar space. Hence, activation and recruitment of polymorphonuclear neutrophils (PMNs) are thought to play a key role in the progression of ALI/ARDS. Neutrophils, which have anti-microbial activity, are the first cells to be recruited to the site of inflammation. This review focuses on the mechanisms of neutrophils in patients with ALIs with respect to attachment, recruitment, adhesion, migration, activation, release of damage mediators, and apoptosis via PMNs.