By N. Tony Eissa, David P. Huston
This reference examines the mobile, molecular, and genetic mechanisms curious about airway irritation, in addition to the pathophysiology, epidemiology, and aetiology of bronchial asthma. It explores recommendations to avoid mobile damage and oxidative tissue harm, inhibit key inflammatory pathways and establish disease-specific goals to lessen the induction, development, and exacerbation of sickness.
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Extra info for Lung Biology in Health & Disease Volume 177 Therapeutic Targets in Airway Inflammation
1%) by the age of 3 years, particularly if there was a family history of allergy (59). Other studies have found consistent results (60). F. Bacterial Infection Recent work has suggested that bacterial infections, especially ones produced by the atypical bacteria Chlamydia pneumoniae, may produce new-onset asthma in adulthood or exacerbation of preexisting asthma. Reports that antibiotic treatment improved symptoms in moderate persistent (61,62) and steroid-dependent asthma (63) suggested a linkage between this atypical bacteria and asthma.
Mechanisms of ß2AR Desensitization III. ß2AR Desensitization and Inflammatory Cell Function 781 782 782 Contents IV. V. VI. VII. xxix ß2AR Phosphorylation and Endocytosis Dynamics of ß2AR Endocytosis and Recycling Intracellular Sorting of ß2Ars Conclusions References 38. Genetic Targets in Asthma 783 785 787 789 790 797 Arjun B. Chatterjee, Timothy D. Howard, and Eugene R. Bleecker I. II. III. IV. V. VI. VII. Introduction Definition of Asthma/Diagnostic Criteria Asthma and Obstructive Lung Disease Phenotype Definition in Genetic Studies Evidence for a Genetic Component in Asthma and Allergy Genetically Identified Biological Targets in Asthma Conclusion References 39.
However, some work suggests that the phenotype of this allele may be dependent upon ethnicity as no association was found in a Japanese population (134). Candidate gene studies have identified point mutations on the ␤2-adrenergic receptor that affect the airways responsiveness to ␤ agonists, but are not necessarily a risk factor for asthma. A point mutation at arginine (Arg) 16 (which normally functions to bind agonist and transmit the signal across the cell membrane to the guanine nucleotide-binding protein) to a glycine substitution has been found in more severe asthma (135).