Current asthma medications, which work by suppressing inflammatory signaling by immune cells or by dilating the airways, can stop working over time. A study from Boston Children’s Hospital, Brigham and Women’s Hospital, and Harvard Medical School supports a surprising alternative approach to controlling asthma: targeting certain sensory nerve endings in the lungs that help drive allergic inflammation.
Reporting online in the journal Neuron on June 25, 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.
“An attractive aspect of targeting nociceptors is that this approach would be most effective when inflammation is already present and should accelerate its resolution,” says Clifford Woolf, MD, PhD, director of the FM Kirby Neurobiology Center at Boston Children’s Hospital and a co-senior investigator on the study.
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