Research ArticleHost-Microbe Interactions

Bacterial d-amino acids suppress sinonasal innate immunity through sweet taste receptors in solitary chemosensory cells

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Science Signaling  05 Sep 2017:
Vol. 10, Issue 495, eaam7703
DOI: 10.1126/scisignal.aam7703

The sweet taste of bacteria

Stimulation of the sweet taste receptor (T1R) in solitary chemosensory cells of the upper respiratory epithelium inhibits the release of antimicrobial peptides by neighboring epithelial cells. In addition to being activated by various sugars, T1R can also be activated by some d-amino acids. Lee et al. found that Staphylococcus species in the nasal cavities of chronic rhinosinusitis patients produced d-Phe and d-Leu, both of which can activate T1R. Treatment of primary human sinonasal epithelial cultures with d-Phe and d-Leu inhibited the release of antimicrobial peptides and increased cell death in response to infection with methicillin-resistant S. aureus. d-Phe and d-Leu, as well as medium conditioned by respiratory isolates of Staphylococcus, inhibited the formation of Pseudomonas aeruginosa biofilms. These findings demonstrate that d-amino acids produced by nasal flora can inhibit innate immune responses through T1R and may shape the microbial community of the airways.

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