Taste disorders, including taste distortion and taste loss, are associated with diseases, aging, and medications and contribute significantly to anorexia, malnutrition, and depression. Despite recent progress in identifying taste receptors and taste signaling proteins, little is known about the underlying mechanisms of taste disorders. Our long-term objective is to elucidate the molecular and cellular basis of gustatory dysfunction. Several lines of evidence suggest that inflammation is an important contributing factor to the pathogenesis of taste disorders. First, taste abnormality is frequently associated with inflammatory conditions, such as infections and autoimmune diseases. Second, inflammatory stimuli can change taste preference and food intake. Third, taste bud cells express receptors and signaling molecules for inflammatory factors. Fourth, we have shown that inflammatory cytokines, such as interferons, can alter gene expression and induce cell death in taste buds. So far, however, how inflammation affects taste sensation remains largely unknown. In this application, we propose to study the mechanisms of inflammation-induced taste disorders in animal models. We are going to pursue the following specific aims: 1) We will study the effects of acute and chronic inflammation on taste bud cell renewal and turnover. 2) We will determine the roles of cytokines in mediating the effects of inflammation on taste bud cell renewal and turnover. 3) We will investigate the effects of inflammation and cytokines on taste function. Results from these studies will be important for understanding the roles of inflammation in taste disorders, which will be useful for developing new treatment strategies. In addition, this research will further our knowledge on the regulatory mechanisms of taste bud cell turnover.
Our research investigates the mechanisms of taste dysfunction, a condition associated with aging, various diseases, and some medications. This research is critical for developing new strategies to prevent and treat such disorders.
|Feng, Pu; Chai, Jinghua; Yi, Huilan et al. (2018) Aggravated gut inflammation in mice lacking the taste signaling protein ?-gustducin. Brain Behav Immun 71:23-27|
|Feng, Pu; Jyotaki, Masafumi; Kim, Agnes et al. (2015) Regulation of bitter taste responses by tumor necrosis factor. Brain Behav Immun 49:32-42|
|Feng, Pu; Chai, Jinghua; Zhou, Minliang et al. (2014) Interleukin-10 is produced by a specific subset of taste receptor cells and critical for maintaining structural integrity of mouse taste buds. J Neurosci 34:2689-701|
|Feng, Pu; Huang, Liquan; Wang, Hong (2014) Taste bud homeostasis in health, disease, and aging. Chem Senses 39:3-16|
|Li, Feng; Ponissery-Saidu, Samsudeen; Yee, Karen K et al. (2013) Heterotrimeric G protein subunit G?13 is critical to olfaction. J Neurosci 33:7975-84|
|Samuel, Douglas B; Carroll, Kathleen M; Rounsaville, Bruce J et al. (2013) Personality disorders as maladaptive, extreme variants of normal personality: borderline personality disorder and neuroticism in a substance using sample. J Pers Disord 27:625-35|
|Feng, Pu; Zhao, Hang; Chai, Jinghua et al. (2012) Expression and secretion of TNF-ýý in mouse taste buds: a novel function of a specific subset of type II taste cells. PLoS One 7:e43140|
|Kim, Agnes; Feng, Pu; Ohkuri, Tadahiro et al. (2012) Defects in the peripheral taste structure and function in the MRL/lpr mouse model of autoimmune disease. PLoS One 7:e35588|
|Feng, Pu; Wang, Hong; Feldman, Roy S et al. (2010) The T cells in peripheral taste tissue of healthy human adults: predominant memory T cells and Th-1 cells. Chem Senses 35:501-9|
|Cohn, Zachary J; Kim, Agnes; Huang, Liquan et al. (2010) Lipopolysaccharide-induced inflammation attenuates taste progenitor cell proliferation and shortens the life span of taste bud cells. BMC Neurosci 11:72|