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The Journal of Neuroscience, October 3, 2007, 27(40):10703-10713; doi:10.1523/JNEUROSCI.3102-07.2007

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Neurobiology of Disease
Inflammation Activates the Interferon Signaling Pathways in Taste Bud Cells

Hong Wang,¹ Minliang Zhou,¹ Joseph Brand,^1,2 and Liquan Huang¹

¹Monell Chemical Senses Center, Philadelphia, Pennsylvania 19104-3308, and ²Department of Biochemistry, School of Dental Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104

Correspondence should be addressed to Liquan Huang, Monell Chemical Senses Center, 3500 Market Street, Philadelphia, PA 19104. Email: lhuang{at}monell.org

Patients with viral and bacterial infections or other inflammatory illnesses often experience taste dysfunctions. The agents responsible for these taste disorders are thought to be related to infection-induced inflammation, but the mechanisms are not known. As a first step in characterizing the possible role of inflammation in taste disorders, we report here evidence for the presence of interferon (IFN)-mediated signaling pathways in taste bud cells. IFN receptors, particularly the IFN- receptor IFNGR1, are coexpressed with the taste cell-type markers neuronal cell adhesion molecule and -gustducin, suggesting that both the taste receptor cells and synapse-forming cells in the taste bud can be stimulated by IFN. Incubation of taste bud-containing lingual epithelia with recombinant IFN- and IFN- triggered the IFN-mediated signaling cascades, resulting in the phosphorylation of the downstream STAT1 (signal transducer and activator of transcription protein 1) transcription factor. Intraperitoneal injection of lipopolysaccharide or polyinosinic:polycytidylic acid into mice, mimicking bacterial and viral infections, respectively, altered gene expression patterns in taste bud cells. Furthermore, the systemic administration of either IFN- or IFN- significantly increased the number of taste bud cells undergoing programmed cell death. These findings suggest that bacterial and viral infection-induced IFNs can act directly on taste bud cells, affecting their cellular function in taste transduction, and that IFN-induced apoptosis in taste buds may cause abnormal cell turnover and skew the representation of different taste bud cell types, leading to the development of taste disorders. To our knowledge, this is the first study providing direct evidence that inflammation can affect taste buds through cytokine signaling pathways.

Key words: inflammation; cytokine; interferon; gene expression; taste bud; taste disorder

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Received Feb. 7, 2007; revised Aug. 20, 2007; accepted Aug. 20, 2007.

Correspondence should be addressed to Liquan Huang, Monell Chemical Senses Center, 3500 Market Street, Philadelphia, PA 19104. Email: lhuang{at}monell.org

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