title: Inflammation activates the interferon signaling pathways in taste bud cells.
abstract: 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-gamma receptor IFNGR1, are coexpressed with the taste cell-type markers neuronal cell adhesion molecule and alpha-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-alpha and IFN-gamma 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-alpha or IFN-gamma 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.
authors.affiliation: Monell Chemical Senses Center, Philadelphia, Pennsylvania 19104-3308, USA.
authors.forename: Hong
authors.initials: H
authors.lastname: Wang
authors.forename: Minliang
authors.initials: M
authors.lastname: Zhou
authors.forename: Joseph
authors.initials: J
authors.lastname: Brand
authors.forename: Liquan
authors.initials: L
authors.lastname: Huang
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D002478:Cells, Cultured; D004848:Epithelium / Q000473:pathology; D005786:Gene Expression Regulation / Q000187:drug effects / Q000502:physiology; D007249:Inflammation / Q000139:chemically induced / Q000150:complications*; D007372:Interferons / Q000235:genetics / Q000378:metabolism* / Q000494:pharmacology; D051379:Mice; D008810:Mice, Inbred C57BL; D018448:Models, Immunological; D011070:Poly I-C; D011134:Polysaccharides; D016760:Proto-Oncogene Proteins c-fos / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D017471:Receptors, Interferon / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction / Q000379:methods; D015398:Signal Transduction / Q000502:physiology*; D013650:Taste Buds / Q000187:drug effects / Q000503:physiopathology*; D013651:Taste Disorders / Q000209:etiology / Q000473:pathology*; D000096743:Interferon gamma Receptor
chemical_list: D007372:Interferons; D011070:Poly I-C; D011134:Polysaccharides; D016760:Proto-Oncogene Proteins c-fos; D012333:RNA, Messenger; D017471:Receptors, Interferon; D000096743:Interferon gamma Receptor