Bronchial Epithelium in Asthma Normal Function Damage and Repair Term Paper

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¶ … asthma is the most common chronic disease of childhood and one of the leading causes of morbidity in children. In the United States, trends of increasing childhood asthma prevalence and morbidity in recent years have been found to disproportionately affect nonwhite children living in urban areas and children living in lower socioeconomic conditions. This study provides a review of the peer-reviewed and scholarly literature to identify normal function, damage and repair of the human bronchia, including a discussion of the normal bronchial epithelium, the bronchial epithelium in asthma, bronchial epithelial inflammation, remodeling, normal epithelial repair and cytokines, tissue factor, tissue factor pathway inhibitor, coagulation factors, tissue-type plasminogen activator, plasminogen-activator-inhibitor, epidermal growth factor, hepatocyte growth factor, and nitric oxide and bronchial epithelial damage in other diseases. A discussion concerning the need for new therapy for asthma is followed by a summary of the research and important findings in the conclusion.

Bronchial Epithelium in Asthma: Normal Function, Damage and Repair

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Today, asthma represents the most common chronic disease among young people, afflicting more than three million children in the United States. There has been an increased incidence of asthma in the United States over the last 25 years that most researchers attribute to changes in environmental conditions. This increased incidence and prevalence of asthma is especially confounding because a number of pharmacological preparations with known efficacy for asthma have been introduced during this same period and researchers continue their search for answers and improved clinical interventions. To help provide an overview of current research findings concerning bronchial epithelium in asthma, this study examines the peer-reviewed and scholarly literature to identify normal function, damage and repair of the human bronchia, including a discussion of the normal bronchial epithelium, the bronchial epithelium in asthma, bronchial epithelial inflammation, remodeling, normal epithelial repair and cytokines, tissue factor, tissue factor pathway inhibitor, coagulation factors, tissue-type plasminogen activator, plasminogen-activator-inhibitor, epidermal growth factor, hepatocyte growth factor, and nitric oxide and bronchial epithelial damage in other diseases. A discussion concerning the need for new therapy for asthma is followed by a summary of the research and important findings in the conclusion.

Review and Discussion

The normal bronchial epithelium

According to a recent study by Kercsmar, Dearborn, Schluchter, Xue, Kirchner, Sobolewski, Greenberg, Vesper and Allan (2006) asthma is the most common chronic disease affecting children today, with more than three million young people in the United States alone suffering from this condition. Moreover, the incidence of childhood asthma has continued to increase over the past several decades in spite of the increasing availability of efficacious medications that have been shown to control chronic symptoms and treating exacerbations (Kercsmar et al. 2006).

Furthermore, the prevalence of asthma and its associated morbidity are inordinately elevated among inner-city children compared to their suburban counterparts, the majority of whom are racial minorities (Wright & Steinbach 2001). For instance, Kercsmar and his associates emphasize that, "African-American children in the United States have a higher prevalence of asthma and greater morbidity as measured by acute care visits and hospitalizations compared with white children" (p. 1574). Notwithstanding the growing body of research into asthma and its associated risk factors, it remains unclear how differences in generally known asthma risk factors including chemical and particulate air pollutants, environmental and in utero tobacco smoke exposure, viral respiratory infections, and home allergen exposure explain recent increases in the prevalence of this disease. In this regard, Wright and Steinbach (2001, p. 1086) add that, "As yet unidentified unique factors may contribute to the higher asthma morbidity and mortality rates seen in inner-city poor minority populations."

There are some age-related changes that typically occur in the normal bronchial epithelium. In this regard, Burke and Laramie report that, "There is a gradual age-related decline in pulmonary function beginning at about age 40. The elastic recoil of the lungs decreases, owing to changes in elastin and collagen. The lung weight is decreased by approximately one fifth, the bronchi harden, and the bronchial epithelium and mucous glands degenerate" (2000, p. 161). The histology of the bronchial epithelium in a normal human lung and the histology of the bronchiolar epithelium of a normal human lung are shown in Figure 1 below.

Figure 1. (a) Histology of the bronchial epithelium of a normal human lung; and (B) Histology of the bronchiolar epithelium of a normal human lung

Source: The National Academy of Sciences 2009 at http://books.nap.edu/books/0309044847 / xhtml/images/img00107.gif

The bronchial epithelium shown as (a) in Figure 1 above is organized as a pseudostratified columnar epithelium that has ciliated and secretory mucous goblet cells which line the surface; in addition, basal cells can be discerned from time to time along the basement membrane (Comparative dosimetry of radon in mines and homes 1991). According to these authorities, "The bronchiolar epithelium is thinner and varies in organization from pseudostratified columnar to cuboidal epithelium, depending on how peripheral it is in the branching of bronchioles. The surface is lined by ciliated cells and goblet cells and/or Clara cells, depending on the level of branching of the bronchioles" (Comparative dosimetry of radon in mines and homes 1991, p. 169).

According to a study by Demoly, Simony-Lafontaine, Chanez, Pujol, Lequeux, Michel and Bousquet (1994), significant changes occur in normal bronchial epithelium cells in response to a variety of antagonists. For instance, these researchers report that, "In chronic inflammatory diseases, cells are recruited but may also derive from local proliferation. In normal bronchial epithelium, under 5% of cells are in cycle but in asthma and chronic bronchitis, proliferation may occur" (Demoly et al. 1994, p. 214). Identification of cycling cells can be achieved through immunohistochemistry using PC10 monoclonal antibody (Demoly et al. 1994). In this regard, in this study, these researchers enumerated PCNA-positive cells (labeling index = LI) in bronchial biopsies of seven healthy smokers (HS), 11 healthy non-smokers (HNS), 30 non-smoking asthmatics (NSA), six smoking asthmatics (SA) and 18 chronic bronchitics (CB) (Demoly et al. 1994). A positive control group was comprised of 20 non-small cell lung cancer patients (Demoly et al. 1994).

These researchers note that ciliated and secretory cells were proliferating cell nuclear antigen-negative, but basal cells were found to be proliferating cell nuclear antigen-positive in one member of the 11 HNS (LI = 0.18 +/- 0.60) (Demoly et al. 1994). None of the seven HS were proliferating cell nuclear antigen-postive, but two of the 30 NSA (LI = 0.05 +/- 0.20), two of the six SA (LI = 2.4 +/- 4.3) and 11 of the 18 CB (LI = 12 +/- 20) were positive for proliferating cell nuclear antigen (Demoly et al. 1994). In sum, these researchers conclude that, "In smokers, proliferating cell nuclear antigen positivity correlated with tobacco consumption (Rho = 0.62, p < 0.0008) and in patients with chronic bronchitis, with the degree of metaplasia (tau = 0.815, p < 0.0001). The submucosa of most subjects showed no proliferating cell nuclear antigen immunoreactivity. These findings suggest that the bronchial mucosa of nonsmokers is not hyperproliferative, even in asthmatics. Tobacco smoking increases proliferating cell nuclear antigen immunoreactivity, possibly leading to the metaplasia of chronic bronchitis" (Demoly et al. 1994, p. 215).

The bronchial epithelium in asthma

According to Spannhake, Reddy, Jacoby, Yu, Saatian and Tian (2002), a number of factors are thought to exacerbate the symptoms associated with asthma, with air pollution and viral infections being regarded as especially significant. These authors add that, "Evidence indicates that each of these respiratory insults individually can increase asthma severity in susceptible individuals" (Spannhake et al. 2002, p. 665). In addition, the growing body of research concerning the causes and incidence of asthma has resulted in a need for interpreting epidemiologic findings concerning the impact of long-term exposure to ozone which is known to cause chronic health effects. In this regard, Levy, Carrothers, Tuomisto, Hammitt and Evans report that, "Evidence from animal and human exposure studies shows that long-term exposure could produce sustained decrements in lung function, particularly in small airway measures. Studies of chronic ozone exposures in monkeys and rats found thickening of the epithelium and interstitium of bronchioles" (2001, p. 1215).

In these experiments, the respiratory epithelium was shown to be replaced by bronchial epithelium in the central acinar region in rats following long-term exposure to ozone (Levy et al. 2001). Consequently, long-term exposure to ozone is believed to cause bronchiolitis with remodeling of the bronchiolar epithelium resulting in a decreased diffusion capacity, fibrosis resulting in a reduction of lung elasticity, and proliferation of type II pneumocytes; these changes in have also been identified in autopsied human lungs following long-term ozone exposure (Levy et al. 2001).

In their study, "Airway mucosal inflammation even in patients with newly diagnosed asthma," Laitinen, Laitinen and Haahtela (1993) analyzed bronchial biopsies from 14 patients who were newly diagnosed with asthma (n=four males; 10 females); on average, the 14 subjects had exhibited asthma symptoms for 7.4 months (range, 2 to 12 months); besides these 14 subjects, these researchers also examined bronchial biopsies from four control subjects (Laitinen et al. 1993). According to these… [END OF PREVIEW] . . . READ MORE

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