Inflammation in COPD

Glucocorticoids have also been used to treat airway inflammation in COPD, but their use in this... 

Kobayashi M, Nasuhara Y, Betsuyaku T, et al. Effect of low-dose theophylline on airway inflammation in COPD. Respirology. 2004 9 249-254. 

Figure 2 Amplification of lung inflammation in COPD. Normal smokers have a mild inflammatory response, which represents the normal (probably protective) reaction of the respiratory mucosa to chronic inhaled irritants.

Cytokines are the mediators of chronic inflammation, and several have been implicated in COPD (7). An increase in concentration of TNF-a is observed in induced sputum in stable COPD with an additional increase during exacerbations (13,17). TNF-a production from peripheral blood monocytes is also increased in COPD patients and has been implicated in the cachexia and skeletal muscle apoptosis found in some patients with severe disease. TNF-a is a potent activator of NF-kB, which may amplify the inflammatory response. Unfortunately anti-TNF therapies have not proved to be effective in COPD patients. IL-ip and IL-6 are other proinflammatory cytokines that may amplify the inflammation in COPD and may be important for systemic circulation. 

TABLE 27—2. Features of Inflammation in COPD Compared with Asthma... 

Yamamoto C, Yoneda T, Yoshikawa M, Fu A, Tokuyama T, Tsukaguchi K, Narita N. Airway inflammation in COPD assessed by sputum levels of interleukin-8. Chest 1997 112 505-510. 

Recent studies demonstrated a significantly increased expression of CXCRl on circulating neutrophils in COPD patients compared to healthy controls [50]. Furthermore, it is established that the expression of CXCR2 in bronchial biopsies of COPD patients is increased [51]. These two receptors have the capacity to regulate the migration of neutrophils into the pulmonary tissue during the neutrophilic inflammation in COPD. Also, activated neutrophils are undoubtedly crucial players in the... 

Inflammation is present in the lungs of all smokers. It is unclear why only 15% to 20% of smokers develop COPD, but susceptible individuals appear to have an exaggerated inflammatory response.5 O The inflammation of COPD differs from that seen in asthma, so the use of anti-inflammatory medications and the response to those medications are different. The inflammation of asthma is mainly mediated through eosinophils and mast cells. In COPD the primary inflammatory cells include neutrophils, macrophages, and CD8+ T lymphocytes. 

The inflammation in asthmatics also causes an associated increase in airway responsiveness to a variety of stimuli. The structural and inflammatory changes of COPD and asthma are described in detail elsewhere. 

Fluticasone Alters gene expression Reduces mediators of inflammation powerful prophylaxis of exacerbations Asthma adjunct in COPD Aerosol duration hours Toxicity Limited by aerosol application candidal infection, vocal cord changes... 

As indicated previously, bronchospasm is often present in COPD—that is, in chronic bronchitis and emphysema.121 Chronic bronchitis is a clinical diagnosis applied to a long-standing inflammation of the bronchial tree. Emphysema is a pathologic condition marked by the destruction of alveolar walls and enlargement of the terminal air spaces. 

Cosio MG, Majo J, Cosio MG. Inflammation of the airways and lung parenchyma in COPD role of T cells. Chest 2002 121 160S-165S. 

Walsh GM., McDougall CM. The resolution of airway inflammation in asthma and COPD. In Progress in Inflammation Research. Rossi AG, Sawatzky D, eds. 2008. Birkhauser Verlag AG, Berhn. pp. 159-191. 

It is helpful to differentiate inflammation occnrring in COPD from that present in asthma because the response to anti-inflammatory therapy differs. The inflammatory cells that predominate differ between the two conditions, with neutrophils playing a major role in COPD and eosinophils and mast cells in asthma. Mediators of inflammation also differ with LTB4, IL-8, and TNF-a predominating in COPD, compared with LTD4, IL-4, and IL-5 among the nnmer-ous mediators modulating inflammation in asthma. Characteristics of inflammation for the two diseases are summarized in Table 27-2. 

Corticosteroid therapy has been studied and debated in COPD therapy for half a century however, owing to the poor risk-benefit ratio, chronic systemic corticosteroid therapy should be avoided if possible. Because of the potential role of inflammation in the pathogenesis of the disease, clinicians hoped that corticosteroids would be promising agents in COPD management. However, their use continues to be debated, especially in the management of stable COPD. 

Figure 6.1 Involvement of chemokines and chemokine receptors and different cell types in the inflammation of COPD. Chemokines released from epithelial cells and macrophages...

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