Smoke concentration also plays an important role.
Book Lung Biology In Health Disease Volume 170 Disease Markers In Exhaled Breath
Hodge-Bell et al. Regarding sex, March et al. CS studies have also been done in rats [ 49 - 54 ]. CS exposure produces not only pulmonary alterations, but also systemic manifestations, such as weight loss [ 55 - 59 ], oxidative modifications of muscle protein in respiratory and limb muscles [ 60 ], reduction of skeletal muscle strength and increase in catabolic factors [ 59 ], systemic inflammation [ 61 ], and pulmonary arterial hypertension [ 62 ] Table 1.
On the other hand, most models cannot reproduce the features of severe emphysema as observed in humans, which would translate into GOLD stages 3 or 4. Usually, only mild features corresponding to GOLD stages 1 or 2 are observed, regardless of exposure time [ 63 ], whereas in humans, the majority of morbidity and mortality occurs in patients with severe disease [ 64 ]. Moreover, all changes induced by CS exposure take time to be observed [ 61 , 65 , 66 ]. Finally, unlike in human advanced COPD, the lesions induced by this model do not progress after cessation of CS exposure.
Jobse et al. Porcine pancreatic elastase PPE offers the advantages of being inexpensive and able to induce features of panacinar emphysema [ 64 , 68 , 69 ] and more widespread lung damage [ 17 ]. A wide variety of studies have highlighted the proteolytic activity of elastase in causing structural changes, such as higher mean linear intercept and alveolar enlargement both in mice [ 71 - 75 ] and in rats [ 76 - 79 ] Table 2.
Furthermore, several studies reported changes in ECM composition after elastase administration, such as disorganized elastin [ 80 , 81 ], degradation of proteoglycans [ 82 ], and abnormal collagen remodeling [ 83 - 88 ]. However, as in CS models, these effects are dependent on several factors, including strain; enzyme dose at each instillation; and number of elastase challenges Figure 2. Limjunyawong et al. Unlike with the nonprogressive CS exposure model, these changes persisted for 6 months after injury induction [ 90 ]. Similar results have been demonstrated by other groups [ 74 , 81 , 82 , 91 - 94 ].
Furthermore, after multiple elastase instillations in mice, Cruz et al. Gain-of-function models have added further proof to the protease-antiprotease imbalance hypothesis [ 97 ]. In this line, mice overexpressing human interstitial collagenase MMP- 1 showed airspace enlargement [ 98 ] and degradation of type III collagen [ 99 , ]. Furthermore, in mice, Wang et al. Targeted mutagenesis also allows investigators to generate strains of COPD mice that lack individual proteins loss-offunction mutations , such as elastin [ ], fibulin-5 [ ], platelet derived growth factor PDGF [ , ], fibroblast growth factor receptor FGFR [ ], surfactant protein-D SP-D [ - ], tissue inhibitor of metalloproteinases-3 TIMP-3 [ ], and ATP binding cassette A3 Abca3 , a lipid transport protein required for synthesis and storage of pulmonary surfactant in type II cells in the alveoli [ ].
Recently, Holm et al. These mice exhibit increased total lung capacity and evidence of a decrease in mean density of the lung parenchyma on breath-hold gated microcomputed tomography micro-TC [ ]. Rangasamy et al. Similarly, Adenuga et al.
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In some mouse strains, spontaneous development of emphysema has been observed in association with genetic abnormalities. In short, gene-targeting techniques are very useful tools to identify the role of distinct genes in the regulation of pulmonary homeostasis and to examine potential mechanisms underlying human COPD [ ]. However, a major disadvantage of these models is that the gene of interest is also expressed in other organs [ 97 ], which can cause systemic effects.
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Frequent acute exacerbations are observed during the life course of COPD patients [ ]. Most exacerbations are triggered by infection, usually viral [ ] or bacterial [ ].
Repeated exacerbations are associated with worse prognosis [ , ], airway inflammation [ ], and lung function impairment [ ] Figure 3. Most exacerbations are caused by viral or bacterial infection. Air pollution and environmental conditions may increase airway inflammation or bronchomotor tone.
Extrapulmonary effects can also increase the risk of exacerbations, as well as mortality. Exacerbations increase lung inflammation, worsen respiratory symptoms and lung function, and accelerate disease progression. The susceptibility of smokers with COPD to respiratory infections is greater than that of nonsmokers, because CS exposure causes several disruptions to the innate lung defenses, such as impairment of mucociliary clearance [ ], reductions in ciliary beat frequency and in the numbers of ciliated cells due to squamous metaplasia [ ], reduction in the concentrations of surfactant proteins A and D [ ], salivary lysozyme and sputum secretory leukocyte protease inhibitor deficiency [ , ], and impairment of phagocytosis by alveolar macrophages [ , ] Figure 4.
In addition, even a stable COPD condition is associated with respiratory pathogens in the airways, which worsens airflow conductance [ , ] and triggers an inflammatory response [ 15 , , - ] and presence of inflammatory markers in sputum [ , - ]. During exacerbations, these inflammatory cells and mediators increase [ , ], as does the H 2 O 2 concentration in exhaled breath condensate [ , ]. Figure 4: Influence of smoking on the function of immune cells throughout the respiratory system.
Therefore, effective strategies to reduce the incidence of COPD exacerbations and their duration are needed. The administration of corticosteroids has long been a mainstay of therapy for acute COPD exacerbations; however, chronic corticosteroid use is associated with many adverse events [ ] and with increased risk of pneumonia, possibly due to their immunosuppressive action [ - ].
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Minimal wear. Shipped to over one million happy customers. See details. Buy It Now. Add to cart. Be the first to write a review About this product. About this product Product Information With nearly references, Disease Markers in Exhaled Breath is essential reading for pulmonologists; anesthesiologists; physiologists; chest, pulmonary, thoracic, and cardiovascular physicians and surgeons; asthmologists; and upper-level undergraduate, graduate, and medical school students in these disciplines.
It discusses the potential diagnostic value of markers in several disorders including cancer, asthma, transplant rejection, and heart disease. Additional Product Features Dewey Edition. Belvisi, Jane A. Mitchell, and Sir Magdi H. Christofer Adding and Lars E. Massaro, Lester Kobzik, George T. De Sanctis, and Jeffrey M.