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Asthmatic airway

Forced expiration is commonly used to assess pulmonary function in both healthy and impaired individuals. Static measures of lung volumes (TLC, Vj, FRC) fail to detect dynamic changes in pulmonary function that are attributable to disease (e.g., asthmatic airway constriction). Obtaining maximum expiratory flow-volume (MEFV) curves (Fig. 5.21) permits derivation of key parameters in detecting changes in lung function. [Pg.210]

Asthma is a complex respiratory disorder that involves mast cell degranulation, mucous secretions, and smooth muscle hypertrophy and hyperresponsiveness. Smooth muscle hyperresponsiveness has suggested some defect in the regulation of smooth muscle contractility. Therefore, a number of studies concerning asthma have centered on whether alterations in the regulation of smooth muscle contraction (Figure 4) are responsible for hyperactivity in asthmatic airway smooth muscle. [Pg.72]

Ying S, O Connor B, Ratoff J, et al. Thymic stromal lymphopoietin expression is increased in asthmatic airways and correlates with expression of Th2-attracting chemokines and disease severity. J Immunol 2005 174(12) 8183—8190. [Pg.249]

Brightling CE, Ammit AJ, Kaur D, et al. The CXCL10/CXCR3 axis mediates human lung mast cell migration to asthmatic airway smooth muscle. Am J Respir Crit Care Med 2005 171(10) 1103-1108. [Pg.252]

Flood-Page PT, Menzies-Gow AN, Kay AB, Robinson DS. EosinophiTs role remains uncertain as anti-interleukin-5 only partially depletes numbers in asthmatic airway. Am J Respir Crit Care Med 2003 167(2) 199-204. [Pg.253]

Joubert P, Lajoie-Kadoch S, Labonte I, et al. CCR3 expression and function in asthmatic airway smooth muscle cells. J Immunol 2005 175(4) 2702-2708. [Pg.254]

Idzko M, Hammad H, van Nimwegen M, Kool M, Willart MA, Muskens F, Hoogsteden HC, Luttmann W, Ferrari D, Di Virgiho F, Virchow JC Jr, Lambrecht BN Extracellular ATP triggers and maintains asthmatic airway inflammation by activating dendritic cells. Nat Med 2007 13 913-919. [Pg.199]

Corticosteroids have been used to treat asthma since 1950 and are presumed to act by their broad anti-inflammatory efficacy, mediated in part by inhibition of production of inflammatory cytokines (see Chapter 39). They do not relax airway smooth muscle directly but reduce bronchial reactivity and reduce the frequency of asthma exacerbations if taken regularly. Their effect on airway obstruction may be due in part to their contraction of engorged vessels in the bronchial mucosa and their potentiation of the effects of 13-receptor agonists, but their most important action is inhibition of the infiltration of asthmatic airways by lymphocytes, eosinophils, and mast cells. [Pg.436]

Bradding P, Roberts JA, Britten KM, Montefort S, et al. 1994. Interleukin-4, -5, and -6 and tumor necrosis factor-alpha in normal and asthmatic airways Evidence for the human mast cell as a source of these cytokines. Am J Respir Cell Mol Biol. 10 471—480. [Pg.55]

Th2 cytokine IL-10 is an antiinflammatory cytokine that suppresses the secretion of proinflammatory cytokines (Dll), allergen-induced airway inflammation, and nonspecific airway responsiveness (T9). IL-13 shares a receptor component, signaling pathways, and many biological activities with IL-4. In fact, IL-13 is also an antiinflammatory cytokine and plays a unique role in the optimal induction and maintenance of IgE production and IgE-mediated allergic responses when IL-4 production is low or absent (DIO, W12). Moreover, IL-13 or IL-4 shows a synergistic effect with TNF-a or IL-5 on eosinophil activation (L20). Recently, IL-11 was found to be involved in the chronic remodeling seen in asthmatic airways and is associated with increasing severity of the disease (Ml6). [Pg.15]

Figure 27.20. Comparison of normal and asthmatic airways. The asthmatic airway is characterized by thickened airway smooth muscle that constricts to cause airway narrowing and obstruction. Mucus secreted by epithelial (goblet) cells also contributes to the obstruction of the airway lumen. (Adapted from Life ART illustration series, Lippincott Williams Wilkins, Hagerstown, MD, 1994. This figure was completely redrawn by the author from materials cited.)... Figure 27.20. Comparison of normal and asthmatic airways. The asthmatic airway is characterized by thickened airway smooth muscle that constricts to cause airway narrowing and obstruction. Mucus secreted by epithelial (goblet) cells also contributes to the obstruction of the airway lumen. (Adapted from Life ART illustration series, Lippincott Williams Wilkins, Hagerstown, MD, 1994. This figure was completely redrawn by the author from materials cited.)...
Bradding, P., Roberts. J.A., Britten. K.M., Montefort. S., Djukanovic, R, Heusser, C.H., Howarth. P.H. and Holgate. S.T. (1994). Interleukins (IL)-4,-5,-6 and TNFa in normal and asthmatic airways evidence for the human mast cell as an important source of these cytokines [Abstract]. Am. J. Respir. Cell Biol. 10, 471-480. [Pg.74]

BAL studies have shown that there is an increase in CD4 lymphocytes, monocytes and eosinophils in asthmatic airways (Walker et al., 1991b). Among the multitude of agents capable of inducing eosinophil migration (Resnick and Weller, 1993), lymphocyte chemotactic factor (LCF Resnick and Weller, 1993), RANTES (Kameyoshi et al., 1992), MlP-la (Rot et al., 1992), MCP-3 (Dahinden etal., 1994), C5a and PAF (Wardlaw... [Pg.88]

Table 5.1 Cytokines present in asthmatic airway BAL fluid... Table 5.1 Cytokines present in asthmatic airway BAL fluid...
IL-5 is of particular interest in the pathophysiology of asthma as it is associated with eosinophilic inflammation (Sanderson, 1992). IL-5 is produced by Tu2-type lymphocytes and there is evidence for increased expression in T lymphocytes in asthmatic airways (Hamid etal., 1991). Endobronchial allergen challenge results in IL-5 mRNA expression in eosinophils in BAL (Broide et al., 1992b) and an increase in IL-5 concentration (Sedgewick et al., 1991 Ohnishi et al., 1993a). Elevated IL-5 concentrations have also been reported in BAL fluid from... [Pg.108]


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