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Asthma susceptibility genes could be "activated" by passive smoking

Susceptibility genes for asthma appear to exert their influence, that is to say, favor the occurrence of signs of the disease, only after being exposed to appropriate environmental stimuli, such as passive smoking, suggests U.S. study published in the "Journal of Allergy and Clinical Immunology" (JACI).
Asthma is a common respiratory disease caused by the interaction of susceptibility genes and environmental factors, remember Deborah Meyers-Wake Forest University in Winston-Salem (North Carolina), which focused on the influence of parental smoking on young children and their subsequent risk of developing asthma.
American researchers have conducted a genetic analysis with 540 people from 200 families with at least one asthmatic parent in families exposed to tobacco smoke on the one hand and in families where this is not the case other.
The proportion of children with asthma (31%) and bronchial hyperresponsiveness (46%) of the participating children confirms the hereditary component of these phenotypes, the authors note.
The results show that bronchial hyperresponsiveness and asthma are associated with chromosomal regions 3p and 5q.
Among families exposed to tobacco smoke, a link to the 5q region has been demonstrated in children with bronchial hyperreactivity, whereas the association with 3p region occurred in both groups. Similar results were obtained for asthma.
These results suggest that passive smoking during early childhood is an environmental factor that interacts with one or more genes located in the chromosome 5q region. These might even need to be exposed to environmental factors such as cigarette smoke, to be expressed and lead to the development of asthma, the authors assume.
However, the prevalence of asthma and bronchial hyperresponsiveness in children appears similar, they were exposed to cigarette smoke or not.

Given the significant results of the genetic analysis, the authors note that this study is not the absence epidemiological and clinical differences should be interpreted with caution.

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Author: Mohammad
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