Asthma susceptibility genes could be "activated" by passive smoking
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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.
Author: Mohammad
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