A study supports a surprising alternative approach to controlling asthma: targeting certain sensory nerve endings in the lungs that help drive allergic inflammation. Current asthma medications, which work by suppressing inflammatory signaling by immune cells or by dilating the airways, can stop working over time. The study was conducted at Boston Children's Hospital, Brigham and Women's Hospital, and Harvard Medical School.
The researchers show that specialized sensory neurons called nociceptors are not only activated by allergic inflammation, but also exacerbate the allergic immune response. When these neurons are selectively silenced in mouse models of acute and chronic asthma, both inflammation and bronchial twitchiness are reduced. Nociceptors in our lungs connect to the brainstem and trigger the cough reflex when they detect potential harms like dust particles, chemical…
