New Insights Into Pathogenesis of Exercise-induced Bronchoconstriction

Teal S. Hallstrand

Disclosures

Curr Opin Allergy Clin Immunol. 2012;12(1):42-48. 

In This Article

Sensory Nerve Involvement in Exercise-induced Bronchoconstriction

An important study[49] using isolated capsaicin-sensitive neurons demonstrated that these neurons respond directly to the CysLT LTD4 via the CysLT1 receptor, and increased the excitability of these neurons to other electrical and chemical stimuli. This study is important because two studies[50,51] conducted in animal models of EIB indicate that the mechanism of bronchoconstriction is mediated through the sensory nerve activation with retrograde axonal transmission via the release of neurokinins. These data are also consistent with our findings in humans that goblet cell mucin 5AC (MUC5AC) is released into the airways during EIB in association with the levels of CysLTs and neurokinin A (NKA) suggesting that CysLTs mediate the activation of sensory nerves and mucus release during EIB in humans.[52]

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