Inflammation Activates the Interferon Signaling Pathways in Taste Bud Cells
Taste bud
Taste receptor
DOI:
10.1523/jneurosci.3102-07.2007
Publication Date:
2007-10-03T16:28:07Z
AUTHORS (4)
ABSTRACT
Patients with viral and bacterial infections or other inflammatory illnesses often experience taste dysfunctions. The agents responsible for these disorders are thought to be related infection-induced inflammation, but the mechanisms not known. As a first step in characterizing possible role of inflammation disorders, we report here evidence presence interferon (IFN)-mediated signaling pathways bud cells. IFN receptors, particularly IFN-γ receptor IFNGR1, coexpressed cell-type markers neuronal cell adhesion molecule α-gustducin, suggesting that both cells synapse-forming can stimulated by IFN. Incubation bud-containing lingual epithelia recombinant IFN-α triggered IFN-mediated cascades, resulting phosphorylation downstream STAT1 (signal transducer activator transcription protein 1) factor. Intraperitoneal injection lipopolysaccharide polyinosinic:polycytidylic acid into mice, mimicking infections, respectively, altered gene expression patterns Furthermore, systemic administration either significantly increased number undergoing programmed death. These findings suggest IFNs act directly on cells, affecting their cellular function transduction, IFN-induced apoptosis buds may cause abnormal turnover skew representation different types, leading development disorders. To our knowledge, this is study providing direct affect through cytokine pathways.
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