Brushing up on lung inflammation
Inhaled environmental allergens elicit type 2 lung inflammation leading to an increase in the risk of developing allergies and asthma. Bankova et al. found that one step along this pathway depends on the lipid mediator leukotriene E4 signaling through a receptor on respiratory epithelial cells to increase the number of brush cells, a rare population of chemosensory cells in the lung epithelium that express receptors shared by taste bud cells. These brush cells were identified as the major pulmonary source for synthesis of interleukin-25 (IL-25), a proinflammatory protein increased in diseases associated with type 2 inflammation. These results highlight the contributions that leukotriene E4 and IL-25 make to the signaling pathways that perpetuate allergic diseases.
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