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Significance Asthma is an inflammatory airway disease characterized by acute attacks in which airway constriction impedes breathing. The variable success of anti-inflammatory treatments in managing asthma attacks suggests that additional mechanisms contribute to this symptom. Here, we used a mouse model of acute asthma to show that a subset of sensory neurons mediates the hyperreactive airway responses. These findings define a cellular substrate outside the immune system that may serve as an important target in the management of asthmatic airway hyperreactivity.
Tränkner et al. (Mon,) studied this question.