Abstract
Asthma is an allergic disease that affects approximately 300 million people worldwide. Two of its phenotypes routinely assessed at the clinic include airway hyperresponsiveness and IgE production. They can be measured in a non-invasive manner and have been used for genetic studies.
The genetic complexity of asthma and its phenotypes makes it difficult to map their genetic contributors. Human studies require large sample sizes and proper segregation of the population to control for potential confounding factors. As an alternative, asthma genetics can be studied in mice due to the high degree of homology in the genome and immune response between mice and humans. The variety of mouse strains and allergic asthma protocols allow to study different aspects of the disease while controlling for the genetic background. Studying the genetic basis of asthma phenotypes has helped gain a better understanding of the disease mechanism. Candidate genes identified from genetic studies have served as targets for the development of new and specialized treatments. New treatments are high in demand as the symptoms of a large number of asthmatics are not properly controlled with the existing treatment guidelines involving corticosteroids, β2-adrenoreceptor agonists, and anti-leukotrienes or leukotriene modifiers. Promising findings have been obtained from studies exploring new treatments targeting specific immune cell mediators, which were identified as candidates in genetic studies, and cell adhesion molecules. In addition to targeting members of the Th1/Th2 inflammatory profile, mediators of the omega-3 fatty acid pathway are also emerging as novel targets of drug intervention for allergic asthma.Keywords: Allergic asthma, asthma genetics, treatments, mouse models, airway hyperresponsiveness, IgE.
Current Pharmaceutical Design
Title:Allergic Asthma: A Summary from Genetic Basis, Mouse Studies, to Diagnosis and Treatment
Volume: 22 Issue: 41
Author(s): Cynthia Kanagaratham and Danuta Radzioch
Affiliation:
Keywords: Allergic asthma, asthma genetics, treatments, mouse models, airway hyperresponsiveness, IgE.
Abstract: Asthma is an allergic disease that affects approximately 300 million people worldwide. Two of its phenotypes routinely assessed at the clinic include airway hyperresponsiveness and IgE production. They can be measured in a non-invasive manner and have been used for genetic studies.
The genetic complexity of asthma and its phenotypes makes it difficult to map their genetic contributors. Human studies require large sample sizes and proper segregation of the population to control for potential confounding factors. As an alternative, asthma genetics can be studied in mice due to the high degree of homology in the genome and immune response between mice and humans. The variety of mouse strains and allergic asthma protocols allow to study different aspects of the disease while controlling for the genetic background. Studying the genetic basis of asthma phenotypes has helped gain a better understanding of the disease mechanism. Candidate genes identified from genetic studies have served as targets for the development of new and specialized treatments. New treatments are high in demand as the symptoms of a large number of asthmatics are not properly controlled with the existing treatment guidelines involving corticosteroids, β2-adrenoreceptor agonists, and anti-leukotrienes or leukotriene modifiers. Promising findings have been obtained from studies exploring new treatments targeting specific immune cell mediators, which were identified as candidates in genetic studies, and cell adhesion molecules. In addition to targeting members of the Th1/Th2 inflammatory profile, mediators of the omega-3 fatty acid pathway are also emerging as novel targets of drug intervention for allergic asthma.Export Options
About this article
Cite this article as:
Kanagaratham Cynthia and Radzioch Danuta, Allergic Asthma: A Summary from Genetic Basis, Mouse Studies, to Diagnosis and Treatment, Current Pharmaceutical Design 2016; 22 (41) . https://dx.doi.org/10.2174/1381612822666160829141708
DOI https://dx.doi.org/10.2174/1381612822666160829141708 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
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