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Airway neurons carry multiple functions in the lungs, ranging from breathing regulation to sensing inhaled noxious particles. In asthma, it appears that these neurons function aberrantly due to being changed after a long period of inflammation, a process called neuroplasticity. Despite advancements in therapy, subsets of patients remain not well controlled. Understanding how neuroplasticity occurs in the asthmatic airways can yield novel druggable targets. Multiple factors can influence this process, such as circulating hormones, such as the ones found in psychological stress exposure, and immune cell-nerve interaction. Thus, we focused on the mechanisms governing neuroplasticity in asthma and associated modulators to understand better the disease pathophysiology and possible intervention opportunities.