Neutrophils and Emerging Targets for Treatment in Chronic Obstructive Pulmonary Disease

Mariska Meijer; Ger T Rijkers; Frans J van Overveld

Disclosures

Expert Rev Clin Immunol. 2013;9(11):1055-1068. 

In This Article

Abstract and Introduction

Abstract

Chronic obstructive pulmonary disease (COPD) is characterized by a decreased airflow due to airway narrowing that, once it occurs, is not fully reversible. The disease usually is progressive and associated with an enhanced inflammatory response in the lungs after exposure to noxious particles or gases. After removal of the noxious particles, the inflammation can continue in a self-sustaining manner. It has been established that improper activation of neutrophils lies at the core of the pathology. This paper provides an overview of the mechanisms by which neutrophils can induce the pulmonary damage of COPD. As the pathogenesis of COPD is slowly being unraveled, new points of intervention are discovered, some of which with promising results.

Introduction

Polymorphonuclear leukocytes are part of the innate immune system and they are part of the myeloid lineage of blood cells, to which also eosinophils and basophils belong. Neutrophils are among the most abundant leukocytes in human beings, with over 1 × 1011 neutrophils generated in the bone marrow on a daily basis, and they have a relatively short lifespan, circulating only 4–10 h before they die.[1] Neutrophils are important cells in the first line of defense. They are the first cells to infiltrate infected and damaged tissues, in order to contain and often clear a broad range of infections in concert with residing tissue macrophages.[2] However, they have also been shown to be the cause of many damaging effects, sometimes in healthy tissue. This is also the case in chronic obstructive pulmonary disease (COPD). This review will discuss how neutrophil activity contributes to the pathogenesis of this disease. It will first give an overview of healthy neutrophil functioning, followed by a discussion on how these same mechanisms can lead to the development of COPD.

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