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ABC of Chronic Obstructive Pulmonary Disease Pathology, Pathogenesis

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ABC of Chronic Obstructive Pulmonary Disease Pathology, Pathogenesis Practice ABC of chronic obstructive pulmonary disease This is the second in a series of 12 articles BMJ: first published as 10.1136/bmj.332.7551.1202 on 18 May 2006. Downloaded from Pathology, pathogenesis, and pathophysiology William MacNee Pathology Chronic obstructive pulmonary disease (COPD) is characterised by poorly reversible airflow obstruction and an abnormal inflammatory response in the lungs. The latter represents the innate and adaptive immune responses to long term exposure to noxious particles and gases, particularly cigarette smoke. All cigarette smokers have some inflammation in their lungs, but those who develop COPD have an enhanced or abnormal response to inhaling toxic agents. This amplified response may result in mucous hypersecretion (chronic bronchitis), tissue destruction (emphysema), and disruption of normal repair and defence mechanisms causing small airway inflammation and fibrosis (bronchiolitis). These pathological changes result in increased resistance to airflow in the small conducting airways, increased compliance of Sagital slice of lung removed from a patient who received a lung the lungs, air trapping, and progressive airflow obstruction—all transplant for COPD. Centrilobular characteristic features of COPD. We have good understanding lesions have coalesced to produce of the cellular and molecular mechanisms underlying the severe lung destruction in the pathological changes found in COPD. upper lobe Pathological changes found in COPD Proximal cartilaginous airways (>2 mm in diameter) Lung parenchyma (respiratory bronchioles and alveoli) x Increased numbers of macrophages and CD8 T lymphocytes x Increased numbers of macrophages and CD8 T lymphocytes x Few neutrophils and eosinophils (neutrophils increase with x Alveolar wall destruction from loss of epithelial and endothelial progressive disease) cells x Submucosal bronchial gland enlargement and goblet cell metaplasia x Development of emphysema (abnormal enlargement of airspaces (results in excessive mucous production or chronic bronchitis) distal to terminal bronchioles) x Cellular infiltrates (neutrophils and lymphocytes) of bronchial x Microscopic emphysematous changes: http://www.bmj.com/ glands Centrilobular—dilatation and destruction of respiratory bronchioles x Airway epithelial squamous metaplasia, ciliary dysfunction, (commonly found in smokers and predominantly in upper zones) hypertrophy of smooth muscle and connective tissue Panacinar—destruction of the whole acinus (commonly found in Peripheral airways (non-cartilaginous airways <2 mm diameter) 1 antitrypsin deficiency and more common in lower zones) x Increased numbers of macrophages and T lymphocytes (CD8 > CD4) x Macroscopic emphysematous changes: x Increased numbers of B lymphocytes, lymphoid follicles, and Microscopic changes progress to bulla formation (defined as an fibroblasts emphysematous airspace > 1 cm in diameter) x Pulmonary vasculature Few neutrophils or eosinophils on 1 October 2021 by guest. Protected copyright. x Bronchiolitis at an early stage x Increased numbers of macrophages and T lymphocytes x Luminal and inflammatory exudates x Early changes—Intimal thickening, endothelial dysfunction x Pathological extension of goblet cells and squamous metaplasia into x Late changes—Hypertrophy of vascular smooth muscle, collagen peripheral airways deposition, destruction of capillary bed, development of x Peribronchial fibrosis and airway narrowing with progressive disease pulmonary hypertension and cor pulmonale Pathogenesis Inflammation is present in the lungs, particularly the small airways, of all people who smoke. This normal protective Cigarette smoke and environmental particles response to the inhaled toxins is amplified in COPD, leading to tissue destruction, impairment of the defence mechanisms that Host factor amplifying mechanisms limit such destruction, and disruption of the repair mechanisms. In general, the inflammatory and structural changes in the Lung inflammation airways increase with disease severity and persist even after Antioxidants Antiproteases smoking cessation. Besides inflammation, two other processes are involved in the pathogenesis of COPD—an imbalance Oxidative Oxidative between proteases and antiproteases and an imbalance between stress stress oxidants and antioxidants (oxidative stress) in the lungs. Effects: Impaired repair Stimulatory Pathological changes of COPD mechanisms Inflammatory cells Inhibitory COPD is characterised by increased numbers of neutrophils, macrophages, and T lymphocytes (CD8 more than CD4) in the The pathogenesis of COPD; dashed bars represent inhibitory effects 1202 BMJ VOLUME 332 20 MAY 2006 bmj.com Practice lungs. In general, the extent of the inflammation is related to Inflammatory cells and mediators in COPD the degree of the airflow obstruction. These inflammatory cells BMJ: first published as 10.1136/bmj.332.7551.1202 on 18 May 2006. Downloaded from release a variety of cytokines and mediators that participate in x Neutrophils, which release proteases, are increased in the sputum and distal airspaces of smokers; a further increase occurs in COPD the disease process. This inflammatory pattern is markedly and is related to disease severity different from that seen in patients with asthma. x Macrophages, which produce inflammatory mediators and proteases, are increased in number in airways, lung parenchyma, Inflammatory mediators and in bronchoalveolar lavage fluid Many inflammatory mediators are increased in COPD, x T lymphocytes (CD4 and CD8 cells) are increased in the airways including and lung parenchyma, with an increase in CD8:CD4 ratio. Numbers x Leucotriene B4, a neutrophil and T cell chemoattractant which of Th1 and Tc1 cells, which produce interferon , also increase. is produced by macrophages, neutrophils, and epithelial cells CD8 cells may be cytotoxic and cause alveolar wall destruction x Chemotactic factors such as the CXC chemokines interleukin x B lymphocytes are increased in the peripheral airways and within lymphoid follicles, possibly as a response to chronic infection of the 8 and growth related oncogene , which are produced by airways. macrophages and epithelial cells. These attract cells from the circulation and amplify pro-inflammatory responses x Pro-inflammatory cytokines such as tumour necrosis factor Proteases and antiproteases involved in COPD and interleukins 1 and 6 x Growth factors such as transforming growth factor , which Proteases Antiproteases may cause fibrosis in the airways either directly or through Serine proteases 1 antitrypsin release of another cytokine, connective tissue growth factor. Neutrophil elastase Cathepsin G Secretory leucoprotease inhibitor Protease and antiprotease imbalance Protease 3 Elafin Increased production (or activity) of proteases and inactivation Cysteine proteases Cystatins (or reduced production) of antiproteases results in imbalance. CathepsinsB,K,L,S Cigarette smoke, and inflammation itself, produce oxidative Matrix metalloproteases Tissue inhibitors of MMP stress, which primes several inflammatory cells to release a (MMP{8, MMP-9, MMP-12) (TIMP1-4) combination of proteases and inactivates several antiproteases by oxidation. The main proteases involved are those produced by neutrophils (including the serine proteases elastase, Effects: Cigarette smoke and other Stimulatory environmental noxious agents cathepsin G, and protease 3) and macrophages (cysteine Inhibitory proteases and cathepsins E, A, L, and S), and various matrix metalloproteases (MMP-8, MMP-9, and MMP-12). The main Epithelial cells Macrophage antiproteases involved in the pathogenesis of emphysema include antitrypsin, secretory leucoprotease inhibitor, and Neutrophil chemotactic factors, 1 cytokines and mediators tissue inhibitors of metalloproteases. CD8 lymphocyte Neutrophil Oxidative stress http://www.bmj.com/ The oxidative burden is increased in COPD. Sources of oxidants include cigarette smoke and reactive oxygen and nitrogen Proteases Protease inhibitors species released from inflammatory cells. This creates an imbalance in oxidants and antioxidants of oxidative stress. Many markers of oxidative stress are increased in stable COPD and Alveolar wall destruction are further increased in exacerbations. Oxidative stress can lead Mucous hypersecretion Oxidants Abnormal tissue repair to inactivation of antiproteases or stimulation of mucous Fibroblast production. It can also amplify inflammation by enhancing on 1 October 2021 by guest. Protected copyright. transcription factor activation (such as nuclear factor B) and Inflammatory mechanisms in COPD. Cigarette smoke activates macrophages hence gene expression of pro-inflammatory mediators. and epithelial cells to release chemotactic factors that recruit neutrophils and CD8 cells from the circulation. These cells release factors that activate fibroblasts, resulting in abnormal repair processes and bronchiolar fibrosis. An imbalance between proteases released from neutrophils and macrophages Pathophysiology and antiproteases leads to alveolar wall destruction (emphysema). Proteases also cause the release of mucous. An increased oxidant burden, resulting from The above pathogenic mechanisms result in the pathological smoke inhalation or release of oxidants from inflammatory leucocytes, causes changes found in COPD. These in turn result in physiological epithelial and other cells to release chemotactic factors, inactivate abnormalities—mucous hypersecretion and ciliary dysfunction, antiproteases, and directly injure alveolar
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