Abstract
Environmental tobacco smoke (ETS) is an environmental trigger that leads to airway inflammation and airway hyperresponsiveness (AHR) in susceptible individuals and animals, but the underlying mechanism is not fully understood. Substance P (SP) release from sensory nerve fibers has been linked to AHR. The present experiments characterize the role of SP in tracheal smooth muscle on ETS-increased airway responses. The mice were exposed to either sidestream tobacco smoke (SS), a surrogate to ETS, or filtered air (FA) for 1 day or 5 consecutive days. Contractions of tracheal smooth muscle to SP and electrical field stimulation (EFS) were not significantly altered in 1 of day SS-exposed mice. However, 5 of days SS exposure significantly increased airway smooth muscle contractions to SP and EFS. Administration of CP-99994, an antagonist of the neurokinin (NK)1 receptor, attenuates the SS exposure-enhanced tracheal smooth muscle responses to EFS. Furthermore, the immunohistochemistry showed that SP nerve fibers were increased in tracheal smooth muscle after 5 of days SS exposure. These results suggest that the increased SP production may contribute to SS-enhanced smooth muscle responsiveness in mice trachea.
Highlights
Environmental tobacco smoke (ETS) is an environmental trigger that leads to airway inflammation and airway hyperresponsiveness (AHR) in susceptible individuals and animals [1,2,3,4,5]
There was no significant difference in the tracheal smooth muscle contraction to Methacholine NFD (MCh) (10−5 M) between 1 day-sidestream tobacco smoke (SS)-exposed (n = 16) mice and filtered air (FA) exposed mice (n = 16) (Figure 2)
5 days of SS exposure slightly increased smooth muscle contraction to MCh, there was no significant difference in airway responses to MCh between 5 days of SS-exposed (n = 30) mice and FA exposed mice (n = 30) (Figure 2)
Summary
Environmental tobacco smoke (ETS) is an environmental trigger that leads to airway inflammation and airway hyperresponsiveness (AHR) in susceptible individuals and animals [1,2,3,4,5]. The airways are innervated through autonomic and sensory nerve fibers [12, 13]. Sensory innervation in the airways is important in the pathogenesis of inflammation associated with asthma. The studies including ours found that increased SP in the airway is involved in cigarette smoke exposure-induced AHR and airway inflammation [2, 18,19,20,21,22,23,24,25]. The role of SP in cigarette smoke exposure-enhanced airway responsiveness is not clear
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