We have shown in nocturnal asthma that alveolar tissue eosinophils are increased at night as compared with the proximal airway, and that they correlate with the overnight decrement in lung function. As the CD4+ cell is thought to be the principal orchestrating cell in eosinophil recruitment, we evaluated its presence in the proximal and distal airways in nocturnal asthma. Eleven patients with nocturnal asthma (NA) and 10 patients with non-nocturnal asthma (NNA) underwent two bronchoscopies with proximal airway endobronchial and distal alveolar tissue transbronchial biopsy in a random order at 4:00 P.M. and at 4:00 A.M. separated by 1 wk. Immunohistochemical staining and morphometric analysis were used to determine the number of CD3+, CD4+, and CD8+ cells and EG2+ eosinophils per mm2 in the epithelium, lamina propria, and alveolar tissue. At 4:00 A.M., the NA group had a significantly greater number of CD4+ cells in the alveolar tissue than the NNA group (9.8 cells/ mm2 [5.6-30.8, interquartile (IQ)] versus 1.5 cells/mm2 [0-6. 3, IQ], p = 0.04). Within the NA group, there were significantly greater numbers of CD3+, CD4+, CD8+, and EG2+ cells in the proximal airway lamina propria than in the distal airway at both 4:00 P.M. and 4:00 A.M. There were no differences within the epithelium between the groups at either time point. Only alveolar tissue, not airway tissue, CD4+ cells correlated inversely with the percentage predicted FEV1 at 4:00 A.M. (r = -0.68, p = 0.0018) and positively with the number of alveolar tissue EG2+ cells (r = 0.66, p = 0.01). These findings suggest that the CD4+ lymphocyte is increased in the alveolar tissue at night in nocturnal asthma as compared with non-nocturnal asthma.
"Z wielu badań, pochodzących głównie z bronchoskopii i biopsji oskrzeli, wynika dość jednoznacznie, że bez względu na kliniczną etiologię astmy oskrzelowej w zapaleniu dominuje naciek złożony z aktywowanych eozynofilów, komórek tucznych i bazofilów z dodatkowym udziałem limfocytów T oraz neutrofilów oraz makrofagów     . Nie ulega żadnych wątpliwości, że liczba neutrofilów i stosunek neutrofilów do eozynofilów jest zmienny. "
[Show abstract][Hide abstract] ABSTRACT: Treatment of asthma has changed over the years. Despite these changes, since the middle of last century many managed to get a consensus to focus the anti-asthma therapy on inflammatory processes. The primary anti-inflammatory medicines for asthma are inhaled glucocorticoids. This paper showed clinical data on inflammation in asthma and summarized the knowledge of novel glucocorticoids used in inhaled asthma therapy. It also highlighted the differences between substances. Currently glucocorticoids are characterized by a very high safety profile and a lot of different inhalation systems. The study highlighted the need to make rational therapeutical choices and proper selection of the drug for the individual patient.
"This suggests that IL-13, which is implicated in the pathogenesis of asthma, has the ability to induce an alveolar remodeling response in asthmatics. In human asthma patients, the numbers of eosinophils, CD4+ T-cells, and macrophages were increased in alveolar tissue at the time symptoms appeared.50,51 Taken together, these data indicate that the destruction of distal airways is a consequence of a chronic, long-lasting injury which can significantly affect lung function in both COPD and asthma. "
[Show abstract][Hide abstract] ABSTRACT: Asthma and chronic obstructive pulmonary disease (COPD) are traditionally recognized as distinct diseases, with some clearly separate characteristic. Asthma originates in childhood, is associated with allergies and eosinophils, and is best treated by targeting inflammation, whereas COPD occurs in adults who smoke, involves neutrophils, and is best treated with bronchodilators and the removal of risk factors. However, the distinction between the two is not always clear. Patients with severe asthma may present with fixed airway obstruction, and patients with COPD may have hyperresponsiveness and eosinophilia. Recognizing and understanding these overlapping features may offer new insight into the mechanisms and treatment of chronic airway inflammatory diseases.
"Airway inflammation in asthma is a multicellular process involving mainly eosinophils, neutrophils, CD4 1 T lymphocytes and mast cells, with eosinophilic infiltration being the most striking feature (Kay 2005) (Fig. 78.1). The inflammatory process is largely restricted to the conducting airways but as the disease becomes more severe and chronic the inflammatory infiltrate spreads both proximately and distally to include the small airways and in some cases adjacent alveoli (Kraft et al. 1999). The inflammatory response in the small airways appears to be predominantly outside the airway smooth muscle (Fig. 78.1), whereas in the large airways inflammation of the submucosa dominates (Haley et al. 1998). "
[Show abstract][Hide abstract] ABSTRACT: While asthma is considered an inflammatory disorder of the conducting airways, it is becoming increasingly apparent that the disease is heterogeneous with respect to immunopathology, clinical phenotypes, response to therapies, and natural history. Once considered purely an allergic disorder dominated by Th2-type lymphocytes, IgE, mast cells, eosinophils, macrophages, and cytokines, the disease also involves local epithelial, mesenchymal, vascular and neurologic events that are involved in directing the Th2 phenotype to the lung and through aberrant injury-repair mechanisms to remodeling of the airway wall. Structural cells provide the necessary "soil" upon which the "seeds" of the inflammatory response are able to take root and maintain a chronic phenotype and upon which are superimposed acute and subacute episodes usually driven by environmental factors such as exposure to allergens, microorganisms, pollutants or caused by inadequate antiinflammatory treatment. Greater consideration of additional immunologic and inflammatory pathways are revealing new ways of intervening in the prevention and treatment of the disease. Thus increased focus on environmental factors beyond allergic exposure (such as virus infection, air pollution, and diet) are identifying targets in structural as well as immune and inflammatory cells at which to direct new interventions.
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.