
By Howard David Pettigrew MD, Christopher Chang MD, Suzanne S. Teuber MD (auth.), M. Eric Gershwin, Timothy E. Albertson (eds.)
Hailed by means of specialist journals and esteemed via basic care physicians, asthma: A consultant for sensible knowing and therapy, 6th version, has been absolutely up to date to aid physicians face the problem of prognosis and administration in each number of sufferer subpopulation.
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Barnes P. Targeting the epigenome in the treatment of asthma and chronic obstructive pulmonary disease. Proc Am Thorac Soc. 2009;6:693–6. Ito K, Ito M, Elliott WM, Cosio B, Caramori G, Kon OM, Barczyk A, Hayashi S, Adcock IM, Hogg JC, Barnes PJ. Decreased histone deacetylase activity in chronic obstructive pulmonary disease. N Engl J Med. 2005 May 12;352(19):1967–76. Kagoshima M, Wilcke T, Ito K, Tsaprouni L, Barnes PJ, Punchard N, Adcock IM. Glucocorticoidmediated transrepression is regulated by histone acetylation and DNA methylation.
Since the first report of an association between ADAM33 polymorphisms and asthma in two Caucasian populations from the UK and the USA, a number of replication studies have been published with differing results (14). The differences in the association results may be due to phenotypic and environmental heterogeneity between cohorts. Additional studies demonstrated that SNPs within the ADAM33 locus are associated with accelerated decline of lung function in the general population and in patients with asthma.
ADAM proteins are involved in cell adhesion, cell fusion, cell signaling, and proteolysis (13). These proteins have the capacity to shed cytokines, growth factors, or their receptors from the cell surface and the remodeling of extracellular matrix components. The enzymatic activity of ADAM33 can be inhibited by tissue inhibitor of metalloproteinase-3 and -4 (TIMP-3 and -4, respectively) as well as several small molecules. This suggests that ADAM33 is involved in pulmonary defenses and tissue remodeling.