IL1B and asthma: The inflammatory cytokines generated during asthma exacerbation, primarily IL-13, can not only directly act on IL-13 and IL-4 receptors on airway SMCs (182), thereby enhancing agonist-evoked excitatory effects by upregulating pro-inflammatory mediators such as IL-1β and TNF-α (183), but also modulate G protein-coupled receptor (GPCR, e.g., muscarinic receptor)-related signaling pathways and/or inhibit cAMP production, thereby altering calcium homeostasis in airway SMCs (184).