People with asthma often experience a worsening of symptoms after eating, but the underlying mechanisms are poorly understood. Dysregulated type 2 immunity in the lung is a known driver of asthma, and ILC2 immune cells have a key role. As food intake is followed by an increase in parasympathetic neurotransmitter release (such as acetylcholine (ACh)), including in the lung, Chen et al. investigated whether postprandial parasympathetic stimulation of type 2 immunity might underlie the food-related exacerbation of asthma-like symptoms in mice.

The authors looked at the effect of food intake in a mouse model of asthma involving intranasally delivered interleukin-33 (IL-33), which induces type 2 immunity in the lung, including the expression of type 2 cytokines in ILC2 cells and eosinophil recruitment. Food intake potentiated these effects and was accompanied by FOS expression in the dorsal motor nucleus of the vagus (DMV), which sends preganglionic parasympathetic cholinergic projections to the lung. Mimicking postprandial parasympathetic activity by chemogenetic activation of the DMV–lung pathway in IL-33-treated mice resulted in ACh release from parasympathetic terminals in the lung and was sufficient to increase type 2 lung immunity by a mechanism dependent on ACh receptors expressed on ILC2 immune cells.