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The Role of Inflammation in the Advancement of Chronic Obstructive Pulmonary Disease. Essay

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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).

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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 & Janciauskiene, 2007), inhibition of TNF-? ene upregulation (Subramaniyam, 2007) and inhibition of lipopolysaccharide activation of monocytes and neutrophil migration (Janciauskiene et al. , 2004). Deficiency of Alpha -1-antitrypsin is associated with COPD progression in both smokers and non-smokers, although far greater in smokers (Bergen et al. , 2010; Fabbri et al. , 2006; Siafakas and Tzortzaki. , 2002; Foos et al. , 2002). Studies have suggested that smoking with this genetic disposition will substantially increase risk of developing COPD (Kohnlein & Welte, 2008; Pauwels & Rabe, 2004; Foos et al. , 2002; Siafakas & Tzortzaki, 2002; Association for

Respiratory Technology and Physiology, 2000). Pathogenesis of COPD Exposure to noxious particles “… triggers cytokine activation to recruit cells, which play a vital role in removing the noxious agents… ” (Nairn & Helbert, 2007, pp22). An infiltration of neutrophils, eosinophils and CD8+ T-lymphocytes into the airways and lungs follows (Demedts et al, 2006; Mahler et al. , 2004; Sopori, 2002). High concentrations of chemokines, interleukon-8 (IL8) and tumor necrosis factor-a have been found in patients with COPD which are potent activators and chemo-attractants of leukocyte subpopulations (Murdoch and Finn, 2000; Yamamoto et al. 1997). The interaction of chemo-attractants with leukocytes initiates a series of coordinated and cellular events, which includes phagocytosis, release of soluble anti-microbials and formation of reactive oxygen compounds involved in intracellular killing (Murdoch & Finn, 2000). Neutrophils and macrophages release elastase, stimulating the production of mucus to assist in ridding the airways of the irritants and subsequent waste generated by the inflammatory response (Shimizu et al. , 2000).

Other processes such as neutrophil necrosis and reactive oxygen species further contribute to mucus hyper secretion (Kim and Nadel, 2004; Mizgerd, 2002). When an inflammatory response is no longer needed protease inhibitor cells dampen the response. Research suggests that the inhibiting response in COPD is not triggered and chronic inflammation presides, representing a crucial mechanism in the pathogenesis of COPD (Demedts et al. , 2006; Hodge et al 2004). Hypersecretion of mucous can inhibit the ciliated epithelium from transporting mucus from the airways.

Subsequent delays in bacteria clearance results in bacterial colonisation, which stimulates further granulocytic recruitment to the airways, escalating the inflammatory response. Chronic inflammation is linked with tissue destruction, imbalance of proteolytic and anti-proteolytic activity, hyper secretion of mucus, increased apoptotic activity and oxidative stress which contribute to the progression of COPD. Long term, chronic inflammation can result in widespread airway and parenchymal cell destruction which further contributes to disease progression (Mantovini et al. 2008; Mohr and Pelletier, 2005; Sattar et al. , 2003; Sopori, 2002; Powells et al. , 2001; Danesh et al. , 2000; Murdoch & Finn, 2000). Research suggests that macrophages express a markedly lower amount of toll like receptors in COPD suffers, resulting in a decreased recognition of microbes, facilitating damaging microbial colonisation, which may explain the increased amount of respiratory infections in COPD sufferers (Schneberger, 2011; Droemann et al. 2005). Infection initiates a biased release of inflammatory mediators which may escalate the pathogenesis of the disease (Gaschler et al. 2009, Ritter et al. , 2005; Sethi, 2000). Oxidative stress Demedts et al, 2005 found that the alveolar macrophages of COPD sufferers produced much higher levers of oxygen radicals and myeloperoxide which are important for the destruction of inter-cellular pathogens. Oxidant/anti-oxidant imbalance can result in the inactivation of anti-proteinases, airspace epithelial injury, increased sequestration of neutrophils in the pulmonary microvasculature, and gene expression of pro-inflammatory mediators, all of which exacerbate the inflammatory response (MacNee, 2000 Drost et al. 2005). Emphysema like changes have been show in the CT scans of malnourished women, suggesting that diet has an effect on lung tissue in the absence of smoking (Coxon et al. , 2004). Dietary supplementation then may be a beneficial therapeutic intervention in this condition, as antioxidants not only protect against the direct injurious effects of oxidants, but fundamentally alter the inflammatory events that play an important part in the pathogenesis of COPD (Coxon et al. , 2004; MacNee, 2000). Apoptosis and COPD

Research suggests that there is increased apoptosis of epithelial cells in smokers and COPD patients. Apoptosis persisted despite smoking cessation which suggests apoptosis may play a part in driving the inflammatory process and progression of the disease (Hodge et al. , 2003). Increased apoptotic alveolar epithelial and endothelial cells in the lungs not counterbalanced by proliferation and sufficient phagocytic clearance results in destruction of lung tissue and development of emphysema (Demedts et al, 2006; Kazutetsu, Naoko & Atsushi, 2003; Barnes et al. 000) Apoptosis can be induced by various stimuli, including oxidative stress, elastase and infiltrating cytoxix CD8 + T cells which are all associated with inflammation (Kazutetsu, Naoko and Atsushi, 2003). Efferocytosis allows for the removal of apoptotic material with minimal inflammation and prevents the development of secondary necrosis and ongoing inflammation. Failure of this highly conserved process may contribute to disease pathogenesis by impeding both the resolution of inflammation and the maintenance of alveolar integrity (Mukaro and Hodge, 2011; Taylor et al. , 2010; Morimoto et al, 2006; Vandivier et al, 2006).

Proteolytic/Anti-proteolytic activity Mukaro and Hodge, (2011) suggests that in COPD there is an imbalance between proteolytic and anti-proteolytic activity, a prominent factor in the pathogenesis of this disease, which may contribute to lung parenchymal destruction. Research has also found that macrophages demonstrate defective phagocytic ability against common airways pathogens in COPD (Taylor et al. , 2010; Hodge et al. , 2003), The findings of Berenson et al. , (2006), supported a paradigm of defective immune responsiveness of alveolar macrophages, but found no significant differences in the blood macrophages of COPD sufferers.

Taylor (2010) believes that persistence of bacteria as a consequence of defective phagocytosis may be a chronic antigenic drive for chronic inflammation. Systemic effects of COPD “Chronic inflammation is present in all disease processes, mediating all stages of disease from initiation, manifestation and maturation” (Sompayrac 2003, pp12). Compelling epidemioligical data links systemic inflammation to atherosclerosis, ischemic heart disease, strokes, and coronary deaths (Danesh, Whincup and Walker, 2000; Ridker, 1999).

These observations have been strongly supported by experiments that show the direct effects of certain inflammatory markers, such as C-reactive protein (CRP), on the pathogenesis of plaque formation (Zwaka, Hombach and Torzewski, 2001; Lagrand, Visser & Hermens, 1999). A study by Gan, Man & Sin, 2003) found that patients with COPD were 2. 18 times more likely to have an elevated circulating c-reactive protein levels. Evidence strongly suggests that there is relationship between COPD, systemic inflammation, and cardiovascular diseases.

Studies show that patients with mild-to-moderate COPD, cardiovascular disease is the leading cause of morbidity and mortality (Din and Man, 2009; Pope et al, 2003). As these diseases share similar risk factors such as smoking, increased age and inactivity, causation is unclear and is likely to be due to multiple factors, including lifestyle, environmental and genetics (Gan, 2005; Agusti et. al. 2003). Discussion Inflammation, it would appear, is a double edged sword; crucial for clearance of pathogens and recovery from injury; but can also contribute to life threatening chronic diseases (Smith, 1994; Sporori, 2003).

COPD is a complex condition, influenced by multiple genetic and/or environmental risks. A cycle of low grade inflammation is the consequence, with destructive and damaging effects, resulting in mucus hyper-secretion, airway obstruction, increased elastase production and oxidative stress, which encourage further inflammation and destruction. COPD is associated with exposure to smoke or noxious gases, however inflammation may also be caused by irritation from coughing, wheezing, respiratory infections and mucus production. Most exacerbations of COPD are caused by bacterial or viral infection (Sanjay and Murphy, 2008; Sanjay 2008).

Mucosal cells produce mucus, which irritates the airways causing airway obstruction. This subsequently reduces FEV1, and cough effectiveness, which contributes to the build up of bacterial mucus. Imbalance between proteolytic and anti-proteolytic activity presides, creating an ideal environment for infection. Research suggests that macrophages express a markedly lower amount of toll like receptors in COPD suffers, resulting in a decreased recognition of microbes, facilitating damaging microbial colonisation, which may explain the increased amount of respiratory infections in COPD sufferers (Schneberger,2011; Droemann et al. 005). Infection initiates a biased release of inflammatory mediators which may escalate the pathogenesis of the disease (Gaschler et al. , 2009, Ritter et al. , 2005; Sethi, 2000). Researchers have found high levels of neutrophils, macrophages and CD8+ cells in ex smokers (Lappers et al. , 2006). Thus, suggesting that inflammatory changes in COPD, although initially induced by inhalation of noxious agents, are fundamental to the disease process, rather than to the initial trigger per se (Gamble et al, 2007). Studies have shown that airway epithelial and T-cell apoptosis in COPD continues despite smoking cessation (Lappers et al. 2006). Excess apoptosis results in inappropriate destruction of host tissue, leading to atrophy and tissue necrosis, which in turn further stimulates the inflammatory response and perpetuates the situation. We have already ascertained an imbalance between the proteolytic and anti-proteolytic activity and this is another factor that contributes, resulting in failure to resolve the inflammatory reaction rapidly (Hodge et al. , 2005). Un-cleared apoptotic cells may undergo secondary necrosis with discharge of injurious cells contents resulting in tissue destruction and further inflammation.

Inability to remove apoptotic cells and debris created overwhelms the normal clearance mechanisms, stimulating further inflammatory responses, further contributing to COPD pathogenesis (Sanjay and Murphy, 2008; Sanjay 2008). It has been identified that the immune system may become less responsive, the longer that chronic inflammation presides, which may lead you to believe that this would initiate an inhibitory effect on the inflammatory process. However this is not the case and the inflammatory process persists, presenting as low level chronic inflammation.

In addition a less responsive immune system is more susceptible to infection, exacerbating the inflammatory response (Sanjay and Murphy, 2008; Sanjay 2008). There appears to be strong epidemiological links between cardiovascular disease and COPD. The same inflammatory markets are evident in both suggesting a systemic link. Both diseases share similar risk factors, so it is difficult to determine initiation of the diseases. One could also argue that the debilitating effects of COPD, which include a reduced exercise capacity, dyspnoea and deconditioning increase the risk of cardiovascular disease development.

In conclusion, it appears that adaptive immune is active in the disease progression of this complex pathophysiological syndrome. Particularly elaboration and production of cytokines, chemical mediators and auto-antibodies, which directly injure respiratory tissues. CD8+ mediates tissue destruction, whereas CD4 orchestrates inflammatory responses, which facilitates humoral immune responses (Gadgill and Duncan 2008). Conclusions made in this review are only valid within the boundaries of the research and papers used. References: Agusti et al (2003) Systemic effects of chronic obstructive pulmonary disease.

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