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Molecular and Cellular Mechanisms Underlying Taste, Smell and Beyond 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: 15 July 2024 | Viewed by 3779

Special Issue Editor


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Guest Editor
Monell Chemical Senses Center, Philadelphia, PA 19104, USA
Interests: taste receptor; taste preferences; feeding behavior; carbohydrate metabolism; adult stem cells
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Special Issue Information

Dear Colleagues,

Taste and smell are two basic senses that enable us to perceive external chemical stimuli. Over the past few decades, by using a variety of experimental models, significant progress has been made towards understanding the molecular, cellular, and circuit mechanisms that underly the perception of taste and olfactory stimuli, ranging from the detection of chemical stimuli by taste, olfactory receptors expressed in taste bud cells, or olfactory sensory neurons to the central information processing in the brain. Yet, many gaps still remain (e.g., how tastants or odorants bind to and activate taste or olfactory receptors; how different brain regions encode the sensory information). Unique to the gustatory and olfactory sensory systems, taste organs and the olfactory epithelium regenerate throughout life. Senescent taste receptor cells or olfactory sensory neurons are replaced by newborn cells generated from adult taste or olfactory stem cells. Recent advances in the relevant fields start to illustrate these processes in detail. Chemosensory signaling elements are not restricted to peripheral taste or olfactory tissues. Emerging evidence demonstrates that they may have key functions in many types of cells outside of the oral and nasal cavities. This brings a new perspective to chemosensory research. In addition to their classical roles in sensing chemicals and triggering behavioral responses, such as the ingestion or rejection of particular foods, taste and smell can also influence many other aspects of physiology. Taste and smell are often understudied in the area of pathophysiology. Yet, many people with COVID-19 suffer from a loss of taste and smell. This can directly impact quality of life and wellness. Understanding taste and smell dysfunction and development of effective treatments are clearly needed. In this research topic, we welcome original research articles and review articles relating to the broader aspect of taste and smell research to help advance the research on chemical senses.

Dr. Peihua Jiang
Guest Editor

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Keywords

  • taste receptor
  • taste preferences
  • feeding behavior
  • carbohydrate metabolism
  • adult stem cells
 

Published Papers (2 papers)

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Research

11 pages, 2136 KiB  
Article
In Vitro Functional Characterization of Type-I Taste Bud Cells as Monocytes/Macrophages-like Which Secrete Proinflammatory Cytokines
by Aziz Hichami, Hamza Saidi, Amira Sayed Khan, Pernelle Degbeni and Naim Akhtar Khan
Int. J. Mol. Sci. 2023, 24(12), 10325; https://doi.org/10.3390/ijms241210325 - 19 Jun 2023
Cited by 1 | Viewed by 1170
Abstract
The sense of taste determines the choice of nutrients and food intake and, consequently, influences feeding behaviors. The taste papillae are primarily composed of three types of taste bud cells (TBC), i.e., type I, type II, and type III. The type I TBC, [...] Read more.
The sense of taste determines the choice of nutrients and food intake and, consequently, influences feeding behaviors. The taste papillae are primarily composed of three types of taste bud cells (TBC), i.e., type I, type II, and type III. The type I TBC, expressing GLAST (glutamate-–aspartate transporter), have been termed as glial-like cells. We hypothesized that these cells could play a role in taste bud immunity as glial cells do in the brain. We purified type I TBC, expressing F4/80, a specific marker of macrophages, from mouse fungiform taste papillae. The purified cells also express CD11b, CD11c, and CD64, generally expressed by glial cells and macrophages. We further assessed whether mouse type I TBC can be polarized toward M1 or M2 macrophages in inflammatory states like lipopolysaccharide (LPS)-triggered inflammation or obesity, known to be associated with low-grade inflammation. Indeed, LPS-treatment and obesity state increased TNFα, IL-1β, and IL-6 expression, both at mRNA and protein levels, in type I TBC. Conversely, purified type I TBC treated with IL-4 showed a significant increase in arginase 1 and IL-4. These findings provide evidence that type I gustatory cells share many features with macrophages and may be involved in oral inflammation. Full article
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19 pages, 8658 KiB  
Article
Adiponectin Enhances Fatty Acid Signaling in Human Taste Cells by Increasing Surface Expression of CD36
by Fangjun Lin, Yan Liu, Trina Rudeski-Rohr, Naima Dahir, Ashley Calder and Timothy A. Gilbertson
Int. J. Mol. Sci. 2023, 24(6), 5801; https://doi.org/10.3390/ijms24065801 - 18 Mar 2023
Cited by 1 | Viewed by 1699
Abstract
Adiponectin, a key metabolic hormone, is secreted into the circulation by fat cells where it enhances insulin sensitivity and stimulates glucose and fatty acid metabolism. Adiponectin receptors are highly expressed in the taste system; however, their effects and mechanisms of action in the [...] Read more.
Adiponectin, a key metabolic hormone, is secreted into the circulation by fat cells where it enhances insulin sensitivity and stimulates glucose and fatty acid metabolism. Adiponectin receptors are highly expressed in the taste system; however, their effects and mechanisms of action in the modulation of gustatory function remain unclear. We utilized an immortalized human fungiform taste cell line (HuFF) to investigate the effect of AdipoRon, an adiponectin receptor agonist, on fatty acid-induced calcium responses. We showed that the fat taste receptors (CD36 and GPR120) and taste signaling molecules (Gα-gust, PLCβ2, and TRPM5) were expressed in HuFF cells. Calcium imaging studies showed that linoleic acid induced a dose-dependent calcium response in HuFF cells, and it was significantly reduced by the antagonists of CD36, GPR120, PLCβ2, and TRPM5. AdipoRon administration enhanced HuFF cell responses to fatty acids but not to a mixture of sweet, bitter, and umami tastants. This enhancement was inhibited by an irreversible CD36 antagonist and by an AMPK inhibitor but was not affected by a GPR120 antagonist. AdipoRon increased the phosphorylation of AMPK and the translocation of CD36 to the cell surface, which was eliminated by blocking AMPK. These results indicate that AdipoRon acts to increase cell surface CD36 in HuFF cells to selectively enhance their responses to fatty acids. This, in turn, is consistent with the ability of adiponectin receptor activity to alter taste cues associated with dietary fat intake. Full article
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