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Expression and Secretion of TNF-α in Mouse Taste Buds: A Novel Function of a Specific Subset of Type II Taste Cells

Public Library of Science
Publication Date
DOI: 10.1371/journal.pone.0043140
  • Research Article
  • Biology
  • Immunology
  • Immune System
  • Cytokines
  • Immunity
  • Inflammation
  • Innate Immunity
  • Microbiology
  • Bacterial Pathogens
  • Gram Positive
  • Host-Pathogen Interaction
  • Molecular Cell Biology
  • Cellular Types
  • Neuroscience
  • Molecular Neuroscience
  • Signaling Pathways
  • Sensory Systems
  • Gustatory System
  • Medicine
  • Anatomy And Physiology
  • Immune Physiology
  • Oral Medicine
  • Oral Diseases
  • Biology
  • Medicine


Taste buds are chemosensory structures widely distributed on the surface of the oral cavity and larynx. Taste cells, exposed to the oral environment, face great challenges in defense against potential pathogens. While immune cells, such as T-cells and macrophages, are rarely found in taste buds, high levels of expression of some immune-response-associated molecules are observed in taste buds. Yet, the cellular origins of these immune molecules such as cytokines in taste buds remain to be determined. Here, we show that a specific subset of taste cells selectively expresses high levels of the inflammatory cytokine tumor necrosis factor-α (TNF-α). Based on immuno-colocalization experiments using taste-cell-type markers, the TNF-α-producing cells are predominantly type II taste cells expressing the taste receptor T1R3. These cells can rapidly increase TNF-α production and secretion upon inflammatory challenges, both in vivo and in vitro. The lipopolysaccharide (LPS)-induced TNF-α expression in taste cells was completely eliminated in TLR2−/−/TLR4−/− double-gene-knockout mice, which confirms that the induction of TNF-α in taste buds by LPS is mediated through TLR signaling pathways. The taste-cell-produced TNF-α may contribute to local immune surveillance, as well as regulate taste sensation under normal and pathological conditions.

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