The Role of Inflammation in the Advancement of Chronic Obstructive Pulmonary Disease.
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
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
References: Barnes P.J (2000) Mechanisms in COPD, Differences from Asthma. Chest, February 2000, vol 117, no. 2, suppl 105-145. [Online] Available at: http://www.ncbi.nlm.nih.gov/pubmed/10673467 (Accessed: 4 November 2011). Kohnlein T. and Welte T. (2008) Alpha-1 Antitrypsin Deficiency: Pathogenesis, Clinical Presentation, Diagnosis, and Treatment, The American Journal of Medicine Volume 121, Issue 1 , Pages 3-9, January 2008 [Online] Mizgerd J.P (2002) Molecular mechanisms of neutrophil recruitment elicited by bacteria in the lungs. Seminars in Immunology. Volume 12 Issue 2 April 2002 Pages 123-132. ------------------------------------------------- Nadel, J.A. (2000) Role of neutrophil elastase in Hypersecretion during COPD exacerbations and proposed therapies. Chest. 2000; 117, 386S-389S. Nairn R & Helbert M (2002) Immunology for Medical Students Smith, J.A. (1994) Neutrophils, host defence and inflammation: a double-edged sword. Journal of Leukocyte Biology. Vol.56 no. 6 672-686 [Online] Available at: http://www.jleukbio.org/content/56/6/672.short (Accessed 20 July 2012). Sompayrac L. (2008) How the Immune System Works. Third edition. Blackwell publishing. Singapore. Sopori M World health organisation (2012) Factsheet Tobacco. Fact sheet N°339. May 2012 [Online] Available at: http://www.who.int/mediacentre/factsheets/fs339/en/index.html (Accessed: 25 July 2012). Yamamoto C