It appears that having airway hyperreactivity is another risk factor for asthma, although researchers are not sure why this is true.

People with pre-existing airway hyperreactivity, such as asthmatics, will react to lower doses of drug.

In addition, ongoing airway inflammation is thought to cause the airway hyperreactivity characteristic of asthma.

This shows that in addition to causing airway hyperreactivity, rhinovirus also promotes the onset of non-atopic asthma.

Another little-understood role of pendrin is in airway hyperreactivity and inflammation, as during asthma attacks and allergic reactions.

Not all people with airway hyperreactivity develop asthma, but in those who do have it, the airway hyperreactivity appears to increase the risk of asthma.

More recently, Bertrand et al suggested a link between familial airway hyperreactivity and premature birth, but Chan et al were unable to support a role of maternal asthma in low birth weight.

Overexpression of IL-17F gene in the airway of mice is associated with airway neutrophilia, the induction of many cytokines, an increase in airway hyperreactivity, and mucus hypersecretion.

Similarly, rhinovirus infection has caused subjects with allergic rhinitis but no history of asthma to have a significantly increased airway hyperreactivity as well as a significantly increased incidence of late asthmatic reactions.