Asthma symptoms are triggered/exacerbated by a range of environmental factors, such as allergens, viruses, fungi, exercise, aspirin, or pollutants. Hitherto considered a disease, asthma is henceforth viewed by many as an environmental syndrome with a heterogeneous pathogenesis. Its diagnostic signature is the reversibility of airway obstruction by drug relaxing the airway smooth muscle (ASM), confirming the importance of this tissue in asthma symptoms. Most asthmatics are also hyperresponsive to a bronchoprovocative challenge with a contractile agonist. However, the involvement of ASM in airway hyperresponsiveness (AHR), apart from its undisputed role in airway responsiveness, is still uncertain. This is mainly due to our inability to assess ASM function in vivo.

The argument that asthmatic ASM is stronger has lost favor when ASM was isolated from the lungs and studied ex vivo. Since other ASM properties, apart from its force-generating capacity, may contribute to the manifestation of AHR (e.g., maximal amount of shortening, velocity of shortening, stiffness, ability to relax, and ability to tolerate or recover from oscillating stresses occurring in vivo due to breathing maneuvers), more comparisons are needed between asthmatic and nonasthmatic ASM. Nevertheless, the current bulk of evidence suggests that the ASM is ‘normal’ in asthmatics but may cause AHR upon activation because of nonmuscle factors, such as the thickening of the airway wall which increases airway narrowing for any given degree of ASM shortening.

Alternatively, the hypercontractile phenotype can be exclusively present in vivo, when the ASM is exposed to asthma triggers and/or inflammatory/immunologic mediators that ensue. In fact, just as the degree of airway responsiveness, which is variable in time and in response to interventions, many ASM properties are not static (fixed) but rather plastic (adaptable). The plasticity of ASM can contribute to the variable component of airway responsiveness and contribute to AHR in asthmatics, not because the ASM is ‘abnormal’ but because it operates in a ‘sick’ environment in which it acquires a hypercontractile phenotype.

We are interested in papers that will either ignite or shed light on this overall imbroglio. Potential topics include, but are not limited to:

• Innovative tools and techniques to assess ASM contractility in vivo or in an ex vivo setting that better mimics the in vivo situation
• Comparison of asthmatic and nonasthmatic ASM properties, from humans or animal models
• Nonmuscle tissues in the development or manifestation of AHR
• Asthma triggers on ASM contractility or Ca²⁺ signaling
• Cytokines or other endogenous mediators that are produced in response to asthma triggers on ASM contractility or Ca²⁺ signaling

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