Category Archives: Pulmonary Function

Structural Changes in Airway Diseases: Long-term Reduction of Pulmonary Function

Structural Changes in Airway Diseases: Long-term Reduction of Pulmonary FunctionHow the structural changes could lead to changes in airway function, however, remains uncertain. It is possible that the changes observed in the airway wall structure in asthma influence the above mechanisms and that the loss of distensibility of the airways or other factors cause a persistent impairment of the smooth-muscle stretch-relaxation protective mechanism.
The Childhood Asthma Management Program study has demonstrated an association between asthma duration and reduced lung function, higher AHR, greater asthma symptomatology, and higher use of P2-agonists. Furthermore, Lange and col-leagues showed an accelerated decline in lung function in asthmatic compared to nonasthmatic subjects, with the decline being more severe in smokers. website

Continue reading

Structural Changes in Airway Diseases: Symptoms

Cartilage degradation can contribute to chronic airway obstruction and allow more powerful bron-choconstriction for a given degree of ASM contraction. Peribronchiolar fibrosis occurring in COPD small airways is believed to lead to centrilobular emphysema, resulting in loss of alveolar attachments and thereby contributing to a loss of elastic recoil and early closure of bronchioles during expiration. It has been proposed that small airway alterations might be the earlier stage of COPD, a theory supported by the clinical observation of isolated abnormalities of forced expiratory flow, midexpira-tory phase in the pulmonary function test of smok-ers. However, this has never been proven.
Continue reading

Structural Changes in Airway Diseases: Functional Consequences of Remodeling

Structural Changes in Airway Diseases: Functional Consequences of RemodelingIt has also been proposed that the remodeling process might be beneficial in airway diseases. Lambert and colleagues suggested that airway wall thickening protects against bronchoconstriction. Peribronchiolar fibrosis correlated with milder COPD stage, suggesting that fibrosis can be protective, preventing narrowing. Collagen deposition in subepithelial matrix may inhibit narrowing by making the airway wall stiffer, representing an additional load on ASM. Hyaluronan and versican deposition in and around the smooth muscle also counteracts airway narrowing and smooth-muscle shortening. Experiments conducted on rat models of allergen-induced asthma have suggested that airway responsiveness may increase following airway inflammation but may decrease with the development of airway remodeling.
Continue reading

Structural Changes in Airway Diseases: Results

Genome screening has led to identification of genes or cluster of genes relevant to asthma and atopy. Among them, a disintegrin and metalloproteinase (ADAM-33) has been a focus of interest in the last few years. ADAM-33 has been linked to asthma in a study of 460 white families. ADAM-33 is a membrane-anchored metalloprotease, and abnormal activity of such enzymes can lead to altered airway function, inflammation, and remodeling. In an expression microarray study using tissue obtained from bronchial biopsies of healthy control subjects and of subjects with allergic asthma, Laprise et al found 79 genes showing significant differences in expression in asthmatic compared to control subjects. This type of analysis can potentially guide future research on physiopathology of asthma. fully
Continue reading

Structural Changes in Airway Diseases: Noninflammatory Mechanisms of Remodeling

Structural Changes in Airway Diseases: Noninflammatory Mechanisms of RemodelingHowever, it is not only the inflammatory or toxic airway insult that could per se trigger an abnormal airway repair process. It has been proposed that an alteration of the relationships between the epithelium and airway myofibroblasts (epithelial/mesenchymal trophic unit) could lead to the structural changes in asthma. According to this hypothesis, epithelial cells present an abnormal response to various stimuli by altering the repair process through epidermal growth factor, TGF, and Th2 cytokine production. If the epithelium/myofibroblast communication is perturbed, it may induce a phenotypic change of myofibroblasts and lead to smooth-muscle proliferation. This perturbed communication in combination with wound healing-associated mechanical stress stimulates the development of differentiated myofibroblasts, which then show a de novo expression of a-smooth-muscle actin and increased expression of ED-A fibronectin. Furthermore, the epithelial/mesenchymal signaling to the airway environment might lead to the proliferation of fibroblasts, microvessels, and nerves and may play a role in the persistence of inflammation.
Continue reading

Structural Changes in Airway Diseases: Research

In COPD, inflammatory and structural cells also produce remodeling-associated cytokines. A few inflammatory mediators seem to play an important role in triggering the cascade of events leading to COPD. IL-8, TNF-a, TGF-, and leukotriene B4 are mostly reported in COPD inflammation. Understanding the exact implication of mediators and finding new pertinent mediators will help to improve our knowledge of COPD pathogenesis. Many of these cytokines have chemotactic properties to inflammatory cells, but little information is available on the mechanisms leading to irreversible bronchial structural alterations in COPD. Pathogenesis of COPD can be summarized as being an induced oxidative stress for epithelial cells and macrophages caused by cigarette smoke. read only

Continue reading

Structural Changes in Airway Diseases: Treatment

Structural Changes in Airway Diseases: TreatmentMMP-9 levels are significantly higher in the sputum of asthmatic patients compared with control subjects, but levels of MMP-9 inhibitor tissue inhibitor metalloproteinase (TIMP)-1 are similar to those found in healthy control subjects. This imbalance between MMP-9 and TIMP-1 leads to a profibrotic MMP-9/TIMP-1 ratio. Moreover, MMP-9 level is increased in asthma exacerbation, and after allergenic challenge, and is decreased by corticosteroids. MMPs are implicated in airway inflammation through their influence on eosinophil trafficking and in airway remodeling not only by matrix reorganization but also by its alteration of the angiogenesis and smooth-muscle hyperplasia processes.
Continue reading

Structural Changes in Airway Diseases: Inflammation-Mediated Remodeling

Th2 lymphocytes, mast cells, and eosinophils are important profibrotic inflammatory cells due to their capacity to express potent profibrotic cytokines. Resident cells such as smooth-muscle cells, epithelial cells, and fibroblasts also have fi-brotic properties through their production of extracellular matrix (ECM) proteins and proteases/antiproteases, expression of cytokines, and stimulation of inflammation. The airway fibrotic process has been linked to many cytokines produced by inflammatory cells as well as structural cells. Among them, TGF-P is the most potent and widely studied profi-brotic cytokine and is mainly produced by eosino-phils. TGF-P increases fibroblast production of ECM proteins including collagen I, collagen III, and fibronectin, and decreases collagenase levels in in vitro models. In in vitro or animal models, IL-4 and IL-13 have shown similar fibrotic properties.

Continue reading

Structural Changes in Airway Diseases: Structural Alterations in Other Airway Diseases

Structural Changes in Airway Diseases: Structural Alterations in Other Airway DiseasesMany structural alterations characterize CF airways. Gobletcell and submucosal gland hyperplasia with extension to bronchioles are seen in CF airways. This leads to mucous overproduction and obstruction of small airways leading to bronchiectasis and bronchiolectasis. Peripheral airways of CF patients show increased thickness of inner-wall and smooth-muscle areas when compared with COPD airways. A greater height of the epithelium is also observed. Under the basal lamina, a dense fibrous deposit of collagens I and III, tenascin, and elastin is seen in bronchial wall of CF. In the submucosa, a degradation process occurs in regard to elastic and collagen fibers. Loss of cartilage is also found in CF airways and is related to the severity of bronchiectasis. CF airways are infiltrated with neutrophils and B- and T-cells. IL-8 and leukotriene B4 are the main inflammatory mediators in CF. These alterations contribute to airflow obstruction and possibly airway hyperresponsiveness. buy-asthma-inhalers-online.com
Continue reading

Structural Changes in Airway Diseases: Structural Alterations in COPD

COPD is characterized by fixed or partly reversible airflow limitation and clinical symptoms such as increased sputum production, cough, wheezing, and dyspnea. Cigarette smoking is its main etiologic factor. COPD encompasses two main phenotypes: chronic bronchitis and emphysema. Chronic bronchitis features are increased sputum production and cough, usually associated with airflow limitation. Emphysema is characterized by a loss of lung parenchyma, with an enlargement of peripheral air spaces. In large and smaller airways, bronchial mucosa of COPD is characterized by squamous-cell metaplasia, loss of epithelial cilia, goblet-cell hyperplasia, mucus gland enlargement, smooth-muscle hypertrophy, and inflammatory cell infiltration (Fig 2). Airway wall fibrosis and stenotic lesions are also observed in small airways and, in addition to a change in the protease-antiprotease balance, are implicated in the development of emphysema. These pathologic modifications translate into an increase in bronchial secretions and airway obstruction. there
Continue reading