Article Text

Download PDFPDF
Factors influencing airway inflammation in chronic obstructive pulmonary disease
  1. Adam Hill,
  2. Simon Gompertz,
  3. Robert Stockley
  1. Department of Respiratory Medicine, Queen Elizabeth Hospital, Birmingham B15 2TH, UK
  1. Professor R Stockleyr.a.stockley{at}

Statistics from

Request Permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.

Airway inflammation in chronic obstructive pulmonary disease (COPD) is currently the subject of rapidly increasing research interest, investigating both the nature of the inflammatory cells and the cytokines present. The data are being used to define and assess the severity, cause, prognosis, and response to treatment of this disease. The collection of spontaneous sputum or the induction of sputum has been used to study inflammation in the larger airways. It remains unclear, however, how these data relate to the pathological processes at the site of airflow obstruction (the small airways and alveolar region). Nevertheless, even the interpretation of the results from the large airways depends on the many factors that will influence the inflammation.

The initial process of sputum collection, sample processing, and the performance of assays in the biological fluids being tested may all influence the results. In addition, airways inflammation may be altered by the patient's clinical state, current treatment, and the nature of the disease (asthma, COPD, or bronchiectasis). Other factors including smoking, α1-antitrypsin (AAT) deficiency, and bacterial colonisation may also affect airways inflammation. Despite these many factors that may influence airways inflammation, many papers currently in the literature do not address them. The purpose of this review is to indicate the influence of these factors on airways inflammation to assist interpretation of the data currently in the literature.



Airway inflammation in asthma is classically related to the eosinophil. Eosinophil granules contain a variety of mediators capable of causing inflammatory damage to the airway epithelium including eosinophil peroxidase (EPO), major basic protein (MBP), eosinophil cationic protein (ECP), metalloproteinases, platelet activating factor, and cysteinyl leukotrienes.1 In addition, the immunological basis of asthma is distinct and reflected in the nature of the cytokines released into the airway.

However, there is some overlap with COPD which may …

View Full Text