Chronic Obstructive Pulmonary Disease Exacerbations (Lung Biology in Health and Disease)

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Similarly, Adenuga et al. 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. Frequent acute exacerbations are observed during the life course of COPD patients [ ].


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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.

Q&A on Chronic Obstructive Pulmonary Disease (COPD)

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 [ - ]. Additionally, inhaled or systemic corticosteroids fail to attenuate chronic inflammation in some patients, due to increased oxidative stress [ , ].

Several studies about the use of specific antibiotics in COPD exacerbations have been conducted [ - ], and it is known that antibiotic therapy can reduce sputum purulence [ ]. On the other hand, such therapy may become ineffective against resistant bacterial strains, especially when treatment is provided in-hospital [ , ]. As previously reported, animal models with different purposes have been developed to elucidate the pathophysiology of COPD exacerbations. There are two major experimental approaches to induction of COPD exacerbations: 1 intratracheal instillation of bacterial lipopolysaccharides LPS and 2 challenge with specific bacterial or viral strains.

Using mice, Stolk et al. Six months later, a severe bronchial mucus cell hyperplasia and persistent increase in mean linear intercept, indicating irreversible tissue destruction, were observed [ ]. Recently, Kobayashi et al. Hardaker et al. Recently, also in a CS model, Li et al. Given that bacteria are the main cause of infections in COPD patients, the majority of studies use bacteria to induce exacerbations in emphysema models. In this line, Gashler et al. In both strains, the authors observed an increase in pulmonary inflammation and lung damage.

COPD: Chronic Obstructive Pulmonary Disease

Huvenne et al. In an investigation of the impact of CS on bacterial clearance and immune inflammatory processes in mice, Drannik et al. Recently, Voss et al. Similar results can be obtained after elastase-induced emphysema. In this line, Pang et al. Furthermore, Wang et al. Finally, Ganesan et al. Moreover, ex vivo macrophages showed deficient phagocytosis, possibly could be caused by decreased expression of scavenger receptor A [ ].

Studies in rats are lacking. To date, very few studies have tried to induce viral infection to mimic COPD exacerbations.


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Bauer et al. No major studies have been conducted in rats using viral infection. Figure 1 illustrates the above concepts related to COPD pathophysiology. Although COPD affects primarily the lungs, it is known to be associated with systemic effects [ 36 ].

Chronic obstructive pulmonary disease | Nature Reviews Disease Primers

The major comorbidities observed in COPD are: cardiovascular impairment, such as pulmonary hypertension and heart failure [ 37 , 38 ] diaphragmatic muscle dysfunction [ 39 ] skeletal muscle wasting [ 40 ] osteoporosis; diabetes [ 41 ] and malnutrition and weight loss [ 42 , 43 ].

These comorbidities reduce patient quality of life [ 43 ] and increase the risk of exacerbations [ 44 ] and mortality [ 45 ]. There are three major experimental approaches for induction of emphysema: CS exposure, elastase instillation, and genetic manipulation. The severity of emphysema induced by the CS exposure model can be influenced by some factors, such as differences in animal strains, smoke concentration, and sex.

Vecchio et al.

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Smoke concentration also plays an important role. 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 , ].

see url 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. In some mouse strains, spontaneous development of emphysema has been observed in association with genetic abnormalities.


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  • 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. Frequent acute exacerbations are observed during the life course of COPD patients [ ].

    Original Research ARTICLE

    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. Inhalation aerosols continue to be the basis for successful lung therapy for several diseases, with therapeutic strategies and the range of technology significantly evolving in recent years. In response, this third edition takes a new approach to reflect the close integration of technology with its Chronic Obstructive Pulmonary Disease Exacerbations covers the definition, diagnosis, epidemiology, mechanisms, and treatment associated with COPD exacerbations.

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