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• © 2004 by Society for Leukocyte Biology Eosinophil degranulation in the allergic lung of mice primarily occurs in the airway lumen .
• However, the degranulation process in the allergic lung of mice is primarily compartmentalized to the airway lumen. Understanding the mechanism of eosinophil degranulation in the airway lumen may provide important insights into how this process occurs in human respiratory diseases. ...

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• Role of CFTR in Airway Disease. ...   Cystic fibrosis (CF) is caused by mutations in the gene encoding the CF transmembrane conductance regulator (CFTR), which accounts for the cAMP-regulated chloride conductance of airway epithelial cells. ... It examines the major themes of the channel hypothesis of CF, which involve impaired regulation of airway surface fluid volume or composition. ... At the airway surface, deletion of CFTR causes hyperabsorption of sodium chloride and a reduction in the periciliary salt and water content, which impairs mucociliary clearance. In submucosal glands, loss of CFTR-mediated salt and water secretion compromises the clearance of mucins and a variety of defense substances onto the airway surface. Impaired mucociliary clearance, together with CFTR-related changes in the airway surface microenvironment, leads to a progressive cycle of infection, inflammation, and declining lung function. ...
• Stimulation of beta 2-Adrenergic Receptor Increases Cystic Fibrosis Transmembrane Conductance Regulator Expression in Human Airway Epithelial Cells through a cAMP/Protein Kinase A-independent Pathway.

• Inhibition of airway remodeling in IL-5–deficient mice .
• To determine the role of IL-5 in airway remodeling, IL-5–deficient and WT mice were sensitized to OVA and challenged by repetitive administration of OVA for 3 months. ... In contrast, IL-5–deficient mice had a significant reduction in the number of peribronchial cells staining positive for major basic protein, which was paralleled by a similar reduction in the number of cells staining positive for TGF-ß, suggesting that eosinophils are a significant source of TGF-ß in the remodeled airway. OVA challenge induced significantly higher levels of airway epithelial Vß6 integrin expression, as well as significantly higher levels of bioactive lung TGF-ß in WT compared with IL-5–deficient mice. Increased airway epithelial expression of Vß6 integrin may contribute to the increased activation of latent TGF-ß. These results suggest an important role for IL-5, eosinophils, Vß6, and TGF-ß in airway remodeling. ...
• The accumulation of peribronchial eosinophils is a prominent feature of airway inflammation in asthma (1). ... In vivo studies performed in either IL-5–deficient mice (4), IL-5–transgenic mice (5), or mice treated with anti–IL-5 Ab’s (6) have suggested an important role for IL-5 in acute allergen-induced eosinophilic inflammation and airway hyperreactivity. In IL-5–deficient mice there is a significant reduction in the level of bronchoalveolar eosinophila following OVA allergen challenge, which is associated with significantly less airway hyperreactivity to methacholine (4). Similarly, mice treated with an anti–IL-5 Ab prior to allergen challenge have significantly less airway eosinophilia and airway responsiveness (6, 7). Not all studies in mice treated with anti–IL-5 Ab’s have shown inhibition of allergen-induced airway responsiveness, however (8). Transgenic mice that have been molecularly engineered to constitutively express IL-5 in the lung epithelium develop accumulation of peribronchial eosinophils, goblet cell hyperplasia, epithelial hypertrophy, focal collagen deposition, and airway hyperresponsiveness to methacholine in the absence of aerosolized antigen challenge (5). Moreover, adoptive transfer of eosinophils directly into the lungs of OVA-challenged IL-5–deficient mice results in restoration of pulmonary eosinophilia equivalent to that observed in OVA-challenged WT mice, as well as restoration of the development of airway hyperresponsiveness (9). ... Thus, in the mouse there is considerable evidence that IL-5 plays a prominent role in the development of acute allergen-induced airway eosinophilia, as well as airway responsiveness in most, but not all studies. ...
• Airway allergen challenge in asthmatics induces expression of IL-5 by T lymphocytes (11) and eosinophils (12), while increased levels of IL-5 and eosinophil granule proteins can be detected in the airway of symptomatic asthmatics (13). Inhalation of IL-5 induces airway eosinophilia and airway hyperreactivity to methacholine in human asthmatics (14). Initial studies with anti–IL-5 in mild asthmatics demonstrated that anti–IL-5 was effective in inhibiting sputum and blood eosinophilia more than 90% but was not effective in inhibiting the late-phase response to allergen challenge or airway hyperreactivity to methacholine (15). Subsequent studies in asthmatics have demonstrated that while anti–IL-5 is effective in inhibiting blood and sputum eosinophils more than 90%, anti–IL-5 only partially inhibited airway eosinophils (approximately 55%) and did not reduce the level of airway staining for major basic protein (MBP) (16). ...

• Airway hyperresponsiveness in asthma: not just a matter of airway inflammation .
• Mechanisms of airway narrowing. ...
• Airway inflammation and airway. ...
• According to the most recent definition, bronchial asthma is a chronic inflammatory disorder of the airways associated with reversible airway obstruction and increased airway responsiveness to a variety of stimuli. 1 An intuitive inference from this definition is that a causal relationship may exist between airway inflammation and airway hyperresponsiveness. Along this line of reasoning, most of the research in the last two decades in this field was aimed at identifying inflammatory cell products possibly responsible for the pathogenesis of bronchial asthma and airway hyperresponsiveness. 2 However, the common observation that the asthmatic airways are equally hyperresponsive to a variety of different stimuli does challenge the idea that a single inflammatory cell or mediator may be central to the pathogenesis of asthma and airway hyperresponsiveness and focuses on the importance of an altered mechanical response of the target organ. This view has been recently corroborated by the finding that airway responsiveness of normal individuals may become similar to that of asthmatics by simply changing the pattern of breathing during the bronchial challenge. 3 It is therefore legitimate to wonder how much of airway hyperresponsiveness is due to inflammation or to inherent predisposing factors. ...
• The aims of the present review are to show that airway narrowing in asthma is the ultimate result of an interaction between complex and multiple mechanisms not necessarily and uniquely related to airway inflammation, and to revisit the evidence on which the theorem "airway inflammation equal to airway hyperresponsiveness" has been constructed. ...
•   Mechanisms of airway narrowing in asthma .
• Mechanisms of airway narrowing. ...
• Airway inflammation and airway. ...
• Airway calibre in vivo is the result of a delicate balance between the force generated by the airway smooth muscle (ASM) and a number of opposing factors. ...
• AIRWAY SMOOTH MUSCLE (ASM).
• Although it is widely accepted that ASM contraction is a major cause for airway obstruction in asthma, there is uncertainty as to whether abnormalities of ASM play any part in the pathogenesis of airway hyperresponsiveness. ... Nevertheless, the smooth muscle of asthmatic airways may be able to generate greater force than normal because of hypertrophy and hyperplasia,7 thus causing excessive airway narrowing. 8 9 Although the thickness of the ASM in the airway wall of asthmatic patients might have been overestimated10 and there is no proof that an increased mass of smooth muscle is associated with an increased force generation capacity,11 the possibility that an increased contractile force developed by ASM might contribute to airway hyperresponsiveness in asthma cannot be ruled out. ...

• Liquid secretion properties of airway submucosal glands .
• The tracheobronchial submucosal glands secrete liquid that is important for hydrating airway surfaces, supporting mucociliary transport, and serving as a fluid matrix for numerous secreted macromolecules including the gel-forming mucins. This review details the essential structural elements of airway glands and summarizes what is currently known regarding the ion transport processes responsible for producing the liquid component of gland secretion. ...
• The submucosal glands of the tracheobronchial airways secrete liquid that is essential for flushing the macromolecular component of gland secretion from the gland ducts and for augmenting airway surface liquid (ASL) volume for the support of mucociliary transport. ... Due to space constraints, however, we will not review the macromolecular component of gland secretion, about which a considerable literature exists owing to its importance in the aetiology of obstructive airway diseases. ...
• Bronchioles, the compliant thin-walled distal airways that contain little cartilage, are aglandular; consequently, there is an abrupt transition in gland expression at the bronchial–bronchiolar junction, which occurs at about 1mm airway diameter (Ballard et al. ... Rabbit airways are devoid of submucosal glands, but they do exhibit numerous shallow pits or depressions in the airway surface in which goblet cells are thought to cluster (Widdicombe et al. ...
• An individual airway gland typically consists of a primary (collecting) gland duct, lateral ducts and numerous secretory tubules (Tos, 1966). ...
• The principal exocrine cells of the airway glands are the mucous and serous cells. ... In adult human airway glands, serous cells outnumber mucous cells by about 50% (Takizawa & Thurlbeck, 1971). ...
• Another technique, pioneered by Quinton (1979), involves drying the airway surface with a stream of gas and then layering the surface with water-equilibrated oil. ...
• 1999), but this agonist has no measurable effect on fluid secretion by porcine airway glands (S. ...
• In addition to Cl– secretion, muscarinic agonists and substance P also stimulate HCO3– secretion from airway glands (Fig. ... In any event, ACh-induced secretion of HCO3– is sufficient to induce measurable alkalinization of an airway perfusate (Inglis et al. ...
• Currently, it is unclear whether the secreted acinar fluid is modified as it passes through the gland ducts to the airway surface. ...
• 2002), and depletion of periciliary fluid with consequent flattening of cilia at the airway surface (Trout et al. ...

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• Airway Inflammation .
• Diseases characterized by airway inflammation, excessive airway secretion, and airway obstruction affect a substantial proportion of the population. ... Much progress has been made in the last decade toward an understanding of the mechanisms underlying chronic airway inflammation; recent work has resulted in several new concepts of the initiation and maintenance of airway inflammation. Airway production of chemokines, cytokines, and growth factors in response to irritants, infectious agents, and inflammatory mediators may play an important role in the modulation of acute and chronic airway inflammation. Lipid mediators may be produced by resident airway cells and by inflammatory cells; production of these mediators may also be altered by inflammatory cytokines. Increased airway obstruction may be related to intercurrent viral respiratory infection and to the induction of airway inflammation and airway hyperreactivity that results from such infection. Furthermore, several models exist to explain the processes by which airway inflammation is perpetuated in diseases such as asthma and chronic bronchitis. These include neurogenic inflammation, the perpetuation of the acute inflammatory response, and cycles of airway epithelial cell-mediated and inflammatory cell-mediated recruitment and activation of inflammatory cells. An understanding of these mechanisms of airway inflammation may provide the clinician with new therapeutic approaches to the treatment of these common and chronic diseases. ...
• Shelhamer (National Institutes of Health (NIH), Bethesda, Maryland): Inflammation of the conducting airways is a feature of lung diseases characterized by airway obstruction and excessive airway secretions. ... In patients with asthma, airway obstruction may be initiated by inflammatory events in the airway 2 , and some investigators have suggested that there may be a correlation between indices of airway inflammation and airway hyperresponsiveness 3 . In the patient with chronic bronchitis, there is a correlation between indices of airway inflammation and airway obstruction 4,5 . The mechanisms of this inflammatory response, the ways in which this response is propagated, and the effects of this response on airway function are subjects for investigation. To further explore the role of airway inflammation in chronic airway disease, we review current concepts of cytokine networks in the airways, modulation of lipid mediator metabolism in the airways, the potential role of viral infection in airway hyperresponsiveness, and mechanisms of chronic airway inflammation in asthma and chronic bronchitis. ...
• Bronchial Epithelial Cell-Cytokine Interactions in Airway Inflammation .
• Levine (NIH): Airway epithelial cells can participate in local cytokine networks and regulate inflammatory airway events by synthesizing and secreting various cytokines that communicate in a paracrine manner with infiltrating inflammatory cells and structural airway cells. Furthermore, airway epithelial cells represent targets for numerous cytokines that regulate the expression of immune and inflammatory airway epithelial cell products. Interactions between airway epithelial cell cytokine products and inflammatory as well as structural airway cells enable the airway epithelium to orchestrate specific inflammatory and immune responses that are important both for normal host defense and the pathogenesis of inflammatory airway disorders such as asthma, acute and chronic bronchitis, bronchiectasis, and cystic fibrosis. ...

• Pharmacotherapy and airway remodelling in asthma? .
• Over the last few decades attention has largely focused on airway inflammation in asthma, but more recently it has been appreciated that there are important structural airway changes which have been grouped together under the term "airway remodelling". ... This review examines the nature of these structural airway changes, the mechanisms of their generation, their potential consequences, and what is known about the ability of anti-asthma treatments to modulate these changes. ...
• Keywords: asthma; airway remodelling; pharmacotherapy.
• It is not clear whether airway remodelling is a normal response to an abnormal injury or, alternatively, whether the remodelling/repair response is itself an abnormal response. ... This review will outline the relevant morphological changes in the airway wall before discussing the possible consequences and reviewing what is known about the potential for pharmacotherapy to prevent or reverse these changes. ...
• WHAT CONSTITUTES AIRWAY REMODELLING?.
• In addition to the inflammatory features mentioned earlier, the airway wall of patients with asthma is usually characterised by a number of structural changes that are grouped together under the umbrella term "airway remodelling". ... These changes are structural although, in the broadest sense, airway remodelling encompasses both structural and functional consequences of altered airway morphology. ...
• Figure 1 Comparison of (A) normal and (B, C) asthmatic airway wall showing epithelial damage, increased smooth muscle, inflammatory cell infiltration, and sub-basement membrane thickening. ...
• Despite the variable preservation of airway epithelium in biopsy and necropsy specimens, careful sampling has revealed enhanced epithelial fragility and increased epithelial damage in asthma,2 and the extent of this abnormality correlates with measures of airway reactivity. ...
• 5,6 Interestingly, patients with rhinitis without asthma also show airway subepithelial fibrosis, although it is less marked than in asthma. ... 8–10 The origin of the myofibroblast remains unclear and is explored further in the section on mechanisms of airway remodelling. ...
• Increased smooth muscle mass within both large and small airway walls has long been recognised and is evident in both fatal and non-fatal cases of asthma. ... Increases in airway smooth muscle (ASM) mass may be due to several factors, including proliferation induced by inflammatory mediators, cytokines and growth factors; work hypertrophy due to repeated episodes of bronchospasm; reduced inhibitory control; and accumulation of enriched plasma in the environment surrounding the ASM. ...
• 18 Enlarged congested mucosal blood vessels may contribute to the increased airway wall thickness described later. ...

• As the air passage continues to narrow, pressure increases in the airway and snoring becomes louder. ...

•   Airway Facilities.

• Acute upper airway infections .

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