The Role of inflammation in the advancement of Chronic Obstructive Pulmonary disease. Introduction
Chronic obstructive pulmonary disease (COPD) is the collective term used for respiratory disease, including chronic bronchitis and emphysema. The disease develops slowly and is often not diagnosed until it is advanced and irreparable damage is evident (Global Initiative for Chronic Obstructive Lung Disease, 2011). The disease is characterised by airflow obstruction and lung parenchyma. Parenchyma, associated with emphysema, is the permanent enlargement of the air spaces distal to the terminal bronchioles, accompanied by airway wall destruction, without obvious fibrosis (Demirjian and Kamangar, 2011; Atsuyasu et al., 2007). Airflow limitation results from loss of elastic recoil and reduced airway tethering. Chronic bronchitis leads to narrowing of airway calibre, increasing airway resistance. Patients may display signs of one or both of these diseases as they frequently occur in association with each other. Common symptoms are wheezing, coughing, shortness of breath on exertion, production of sputum and recurrent respiratory infections (Global Initiative for Chronic Obstructive Lung Disease, 2011). There are a host of triggers that exacerbates symptoms including smoking and environmental pollutants, resulting in chronic inflammation (Kazuhiro and Barnes, 2009; Manuel et al., 2002).
“Inflammation is defined as the presence of redness, swelling and pain, caused
by the presence of edema fluid and the infiltration of tissues by leukocytes”
(Nairn & Helbert, 2002, pp15).
Inflammation is a key biological response to eliminate harmful pathogens, but there is increasing evidence to suggest that chronic inflammatory responses are accountable for the advancement of this disease and other chronic diseases including coronary artery disease, cancer, rheumatoid arthritis and multiple sclerosis. This review explores the correlation between COPD and inflammation and the subsequent effects on the systemic systems and the link with coronary heart disease (Mantovini et. al., 2008; Mohr & Pelletier, 2005; Sattar et. al., 2003; Powells et. al., 2001; Danesh et. al., 2000; Murdoch & Finn, 2000). Methods
Search engines used were Google Scholar and Pub Med using the keywords COPD, inflammation, disease, apoptosis, interleukin 8, cytokines, coronary heart disease and COPD. Searches were restricted to dates between 1999 and 2012. The majority of the included papers were obtained from the reference lists of other research papers. COPD risk factors:
COPD is strongly linked with repeated exposure to noxious particles or gases and cigarette smoke has been acknowledged as a prime risk factor (Fabri et. al., 2006; Lindberg et al., 2005; Pauwels and Rabe., 2004, Association for Respiratory Technology & Physiology, 2000). Smokers have an increased prevalence of respiratory and lung function abnormalities, a greater rate of decline in FEV1 and a higher mortality rate than non-smokers (World health organisation, 2012). However, only a third of smokers develop COPD which implies that other factors such as genetics and environment are involved (Agusti, 2003). Exposure to air pollution caused by heating and cooking with bio-mass fuels in poorly ventilated housing are major risk factors for COPD, especially in developing countries (Pauwels & Rabe, 2004). The most documented COPD genetic risk factor is the deficiency of Alpha -1-antitrypsin, a polymorphic glycoprotein which offers anti-protease protection against the serine proteinease, neutrophil elastase (Abboud & Vimalanathan, 2008; Devereux, 2006; Siafakas & Tzortzaki, 2002; Fabbri et al., 2006). Research studies (in vitro) indicated that Alpha – 1 – antitrypsin also possesses anti-inflammatory capabilities that extend beyond its anti-protease role, including regulation of CD14 expression (Nita, Serapinas &...
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