Inflammation and taste disorders: mechanisms in taste buds.
Inflammation and taste disorders: mechanisms in taste buds.
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DOI:
10.1111/j.1749-6632.2009.04480.x
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发表时间:
2009-07
影响因子:
5.2
通讯作者:
Huang L
中科院分区:
文献类型:
--
作者:
Wang H;Zhou M;Brand J;Huang L
Taste disorders, including taste distortion and taste loss, negatively impact general health and quality of life. To understand the underlying molecular and cellular mechanisms, we set out to identify inflammation-related molecules in taste tissue and to assess their role in the development of taste dysfunctions. We found that 10 out of 12 mammalian Toll-like receptors (TLRs), type I and II interferon (IFN) receptors and their downstream signaling components are present in taste tissue. Some TLRs appear to be selectively or more abundantly expressed in taste buds than in non-gustatory lingual epithelium. Immunohistochemistry with antibodies against TLRs 1, 2, 3, 4, 6 and 7 confirmed the presence of these receptor proteins in taste bud cells, of which TLRs 2, 3 and 4 are expressed in the gustducin-expressing type II taste bud cells. Administration of TLR receptor ligands, lipopolysaccharide (LPS) and double-stranded RNA (dsRNA) polyinosinic: polycytidylic acid (poly(I:C)) that mimics bacterial or viral infection, activates the IFN signaling pathways, up-regulates the expression of IFN-inducible genes but down-regulates the expression of c-fos in taste buds. Finally, systemic administration of IFNs augments apoptosis of taste bud cells in mice. Taken together, these data suggest that TLR and IFN pathways function collaboratively in recognizing pathogens and mediating inflammatory responses in taste tissue. This process, however, may interfere with normal taste transduction and taste bud cell turnover and contributes to the development of taste disorders.
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