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Inflammation in asthma

Bousquet J, Chanez P, Vignola AM, Lacoste JY, Michel FB. Eosinophil inflammation in asthma. Am J Respir Crit Care Med 1994 150 S33-38. [Pg.230]

Blake KV. Drug treatment of airway inflammation in asthma. Pharmacotherapy 2001 21 3S-20S. [Pg.230]

A3 receptors are present on human eosinophils and couple to signalling pathways that lead to cell activation ( Kohno et al. 1996a Reeves et al. 2000). Despite this it has not proven easy to demonstrate the functional consequences of activation of these sites (Reeves et al. 2000). Nevertheless, the chronic inflammation in asthma is characterised by extensive infiltration of the airways by activated eosinophils (Holgate 1999 Pearlman 1999) and it remains possible that the elevated adenosine concentrations associated with asthma would contribute to eosinophil activation through stimulation of A3 receptors. In addition, it has been speculated that activation of A3 receptors may protect eosinophils from apoptosis (Gao et al. 2001). Thus, blockade of A3 receptors may reduce the numbers of eosinophils and their activation thereby reducing the pro-inflammatory burden in the lung. Consistent with this, following 6 weeks treatment of mild asthmatics with theophylline there was a... [Pg.240]

Busse WW, Coffman RL, Gelfand EW, Kay AB, et al. 1995. Mechanisms of persistent airway inflammation in asthma. A role for T cells and T-cell products. Am J Respir Crit Care Med. 152 388-393. [Pg.143]

Joos GF, DeSwert KO, Schelfhout V, Pauwels RA. 2003. The role of neural inflammation in asthma and chronic obstructive pulmonary disease. Ann NY Acad Sci. 992 218-230. [Pg.144]

Much inflammation in asthma is thought to be a consequence of the inappropriate accumulation of eosinophils and the subsequent release of their potent proinflammatory arsenal that includes such diverse elements as granule-derived basic proteins, mediators, cytokines, and chemokines (5). Interleukin (lL)-5 is cmcial to the development and release of eosinophils from the bone marrow, their enhanced adhesion to endothelial cells that line the postcapillary venules, and their persistence, activation, and secretion in the tissues. Several animal models of asthma including the use of primates have provided good evidence... [Pg.2328]

Walsh GM., McDougall CM. The resolution of airway inflammation in asthma and COPD. In Progress in Inflammation Research. Rossi AG, Sawatzky D, eds. 2008. Birkhauser Verlag AG, Berhn. pp. 159-191. [Pg.2332]

Varner A, Busse W 1996 Are you undertreating inflammation in asthma Journal of Respiratory Disease 17 656-668 Viel L 1999 Therapeutic efficacy of inhaled fluticasone propionate in horses with chronic obstructive pulmonary disease. In Proceedings of the 45th American Association of Equine Practitioners Annual Convention, Albuquerque, NM, pp. 306-307 Votion D, Ghafir Y, Munsters K et al 1997 Aerosol deposition in equine lungs following ultrasonic nebulisation versus jet aerosol delivery system. [Pg.325]

The degree of inflammation in asthma may vary among individuals because of interaction of genetic and environmental factors [6]. Accordingly, asthma severity is classified as mild, moderate, or severe based on symptoms, lung function, frequency of exacerbation, and physical activity (Table 1). [Pg.162]

It is helpful to differentiate inflammation occnrring in COPD from that present in asthma because the response to anti-inflammatory therapy differs. The inflammatory cells that predominate differ between the two conditions, with neutrophils playing a major role in COPD and eosinophils and mast cells in asthma. Mediators of inflammation also differ with LTB4, IL-8, and TNF-a predominating in COPD, compared with LTD4, IL-4, and IL-5 among the nnmer-ous mediators modulating inflammation in asthma. Characteristics of inflammation for the two diseases are summarized in Table 27-2. [Pg.540]

Bousquet J, Chanez P, Lacoste JY, Bameon G, Ghavanian N, Enander I, Venge P, Ahlstedt S, Simony-Lafontaine J, Godard P, et al Eosinophilic inflammation in asthma. N Engl J Med 1990 323 1033-1039. [Pg.80]

Grunberg K, PJ Sterk. 1999. Rhino virus infections induction and modulation of airways inflammation in asthma. Clin Exp Allergy 29 (suppl 2) 65. [Pg.96]

Wasserman, S. I. (1989) Mast cell-mediated inflammation in asthma. Ann. Allergy63,546-550. [Pg.118]


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See also in sourсe #XX -- [ Pg.906 ]

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