Abstract
The physiological role of airway smooth muscle remains highly elusive given the poor overall understanding of the regulatory elements and their influence in healthy humans [1]. Paradoxically, the pathophysiological contribution of airway smooth muscle contraction to asthma is better understood than the physiological role of this contraction in non-asthmatics: early and late asthmatic responses highlight immediate-immune cell-free and delayed-immune cell-dependent bronchoconstriction, respectively [2]. Reducing the late asthmatic response with the inhaled anti-TSLP antibody ecleralimab raises more questions than providing answers <https://bit.ly/3vOkEIN> We thank David Manley for revising the English in this editorial.
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