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Hong Wang - One of the best experts on this subject based on the ideXlab platform.
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Lipopolysaccharide-induced inflammation attenuates Taste progenitor Cell proliferation and shortens the life span of Taste Bud Cells
BMC Neuroscience, 2010Co-Authors: Zachary J Cohn, Liquan Huang, Joseph Brand, Hong WangAbstract:Background The mammalian Taste Bud, a complex collection of Taste sensory Cells, supporting Cells, and immature basal Cells, is the structural unit for detecting Taste stimuli in the oral cavity. Even though the Cells of the Taste Bud undergo constant turnover, the structural homeostasis of the Bud is maintained by balancing Cell proliferation and Cell death. Compared with nongustatory lingual epithelial Cells, Taste Cells express higher levels of several inflammatory receptors and signalling proteins. Whether inflammation, an underlying condition in some diseases associated with Taste disorders, interferes with Taste Cell renewal and turnover is unknown. Here we report the effects of lipopolysaccharide (LPS)-induced inflammation on Taste progenitor Cell proliferation and Taste Bud Cell turnover in mouse Taste tissues. Results Intraperitoneal injection of LPS rapidly induced expression of several inflammatory cytokines, including tumor necrosis factor (TNF)-α, interferon (IFN)-γ, and interleukin (IL)-6, in mouse circumvallate and foliate papillae. TNF-α and IFN-γ immunoreactivities were preferentially localized to subsets of Cells in Taste Buds. LPS-induced inflammation significantly reduced the number of 5-bromo-2'-deoxyuridine (BrdU)-labeled newborn Taste Bud Cells 1-3 days after LPS injection, suggesting an inhibition of Taste Bud Cell renewal. BrdU pulse-chase experiments showed that BrdU-labeled Taste Cells had a shorter average life span in LPS-treated mice than in controls. To investigate whether LPS inhibits Taste Cell renewal by suppressing Taste progenitor Cell proliferation, we studied the expression of Ki67, a Cell proliferation marker. Quantitative real-time RT-PCR revealed that LPS markedly reduced Ki67 mRNA levels in circumvallate and foliate epithelia. Immunofluorescent staining using anti-Ki67 antibodies showed that LPS decreased the number of Ki67-positive Cells in the basal regions surrounding circumvallate Taste Buds, the niche for Taste progenitor Cells. PCR array experiments showed that the expression of cyclin B2 and E2F1, two key Cell cycle regulators, was markedly downregulated by LPS in the circumvallate and foliate epithelia. Conclusions Our results show that LPS-induced inflammation inhibits Taste progenitor Cell proliferation and interferes with Taste Cell renewal. LPS accelerates Cell turnover and modestly shortens the average life span of Taste Cells. These effects of inflammation may contribute to the development of Taste disorders associated with infections.
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lipopolysaccharide induced inflammation attenuates Taste progenitor Cell proliferation and shortens the life span of Taste Bud Cells
BMC Neuroscience, 2010Co-Authors: Zachary J Cohn, Liquan Huang, Joseph G Brand, Agnes Kim, Hong WangAbstract:Background The mammalian Taste Bud, a complex collection of Taste sensory Cells, supporting Cells, and immature basal Cells, is the structural unit for detecting Taste stimuli in the oral cavity. Even though the Cells of the Taste Bud undergo constant turnover, the structural homeostasis of the Bud is maintained by balancing Cell proliferation and Cell death. Compared with nongustatory lingual epithelial Cells, Taste Cells express higher levels of several inflammatory receptors and signalling proteins. Whether inflammation, an underlying condition in some diseases associated with Taste disorders, interferes with Taste Cell renewal and turnover is unknown. Here we report the effects of lipopolysaccharide (LPS)-induced inflammation on Taste progenitor Cell proliferation and Taste Bud Cell turnover in mouse Taste tissues.
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inflammation activates the interferon signaling pathways in Taste Bud Cells
The Journal of Neuroscience, 2007Co-Authors: Hong Wang, Minliang Zhou, Joseph G Brand, Liquan HuangAbstract:Patients with viral and bacterial infections or other inflammatory illnesses often experience Taste dysfunctions. The agents responsible for these Taste disorders are thought to be related to infection-induced inflammation, but the mechanisms are not known. As a first step in characterizing the possible role of inflammation in Taste disorders, we report here evidence for the presence of interferon (IFN)-mediated signaling pathways in Taste Bud Cells. IFN receptors, particularly the IFN-gamma receptor IFNGR1, are coexpressed with the Taste Cell-type markers neuronal Cell adhesion molecule and alpha-gustducin, suggesting that both the Taste receptor Cells and synapse-forming Cells in the Taste Bud can be stimulated by IFN. Incubation of Taste Bud-containing lingual epithelia with recombinant IFN-alpha and IFN-gamma triggered the IFN-mediated signaling cascades, resulting in the phosphorylation of the downstream STAT1 (signal transducer and activator of transcription protein 1) transcription factor. Intraperitoneal injection of lipopolysaccharide or polyinosinic:polycytidylic acid into mice, mimicking bacterial and viral infections, respectively, altered gene expression patterns in Taste Bud Cells. Furthermore, the systemic administration of either IFN-alpha or IFN-gamma significantly increased the number of Taste Bud Cells undergoing programmed Cell death. These findings suggest that bacterial and viral infection-induced IFNs can act directly on Taste Bud Cells, affecting their Cellular function in Taste transduction, and that IFN-induced apoptosis in Taste Buds may cause abnormal Cell turnover and skew the representation of different Taste Bud Cell types, leading to the development of Taste disorders. To our knowledge, this is the first study providing direct evidence that inflammation can affect Taste Buds through cytokine signaling pathways.
Linda A. Barlow - One of the best experts on this subject based on the ideXlab platform.
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onset of Taste Bud Cell renewal starts at birth and coincides with a shift in shh function
bioRxiv, 2020Co-Authors: E J Golden, Eric D Larson, L A Shechtman, G D Trahan, D Gaillard, T J Fellin, J K Scott, Kenneth L Jones, Linda A. BarlowAbstract:Embryonic Taste Bud primordia are specified as Taste placodes on the tongue surface and differentiate into the first Taste receptor Cells (TRCs) at birth. Throughout adult life, TRCs are continually regenerated from epithelial progenitors. Sonic hedgehog (SHH) signaling regulates TRC development and renewal, repressing Taste fate embryonically, but promoting TRC differentiation in adults. Here we show TRC renewal initiates at birth and coincides with onset of SHHs pro-Taste function. Using transcriptional profiling to explore molecular regulators of renewal, we identified Foxa1 and Foxa2 as potential SHH target genes in lingual progenitors at birth, and show SHH overexpression in vivo alters FOXA1 and FOXA2 expression relevant to Taste Buds. We further bioinformatically identify genes relevant to Cell adhesion and Cell locomotion likely regulated by FOXA1;FOXA2, and show expression of these candidates is also altered by forced SHH expression. We present a new model where SHH promotes TRC differentiation by regulating changes in epithelial Cell adhesion and migration.
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β-catenin is required for Taste Bud Cell renewal and behavioral Taste perception in adult mice.
PLOS Genetics, 2017Co-Authors: Dany Gaillard, Spencer G. Bowles, Ernesto E. Salcedo, Sarah E Millar, Mingang Xu, Linda A. BarlowAbstract:Taste stimuli are transduced by Taste Buds and transmitted to the brain via afferent gustatory fibers. Renewal of Taste receptor Cells from actively dividing progenitors is finely tuned to maintain Taste sensitivity throughout life. We show that conditional β-catenin deletion in mouse Taste progenitors leads to rapid depletion of progenitors and Shh+ precursors, which in turn causes Taste Bud loss, followed by loss of gustatory nerve fibers. In addition, our data suggest LEF1, TCF7 and Wnt3 are involved in a Wnt pathway regulatory feedback loop that controls Taste Cell renewal in the circumvallate papilla epithelium. Unexpectedly, Taste Bud decline is greater in the anterior tongue and palate than in the posterior tongue. Mutant mice with this regional pattern of Taste Bud loss were unable to discern sweet at any concentration, but could distinguish bitter stimuli, albeit with reduced sensitivity. Our findings are consistent with published reports wherein anterior Taste Buds have higher sweet sensitivity while posterior Taste Buds are better tuned to bitter, and suggest β-catenin plays a greater role in renewal of anterior versus posterior Taste Buds.
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β-Catenin Signaling Biases Multipotent Lingual Epithelial Progenitors to Differentiate and Acquire Specific Taste Cell Fates.
Public Library of Science (PLoS), 2015Co-Authors: Dany Gaillard, Sarah E Millar, Fei Liu, Linda A. BarlowAbstract:Continuous Taste Bud Cell renewal is essential to maintain Taste function in adults; however, the molecular mechanisms that regulate Taste Cell turnover are unknown. Using inducible Cre-lox technology, we show that activation of β-catenin signaling in multipotent lingual epithelial progenitors outside of Taste Buds diverts daughter Cells from a general epithelial to a Taste Bud fate. Moreover, while Taste Buds comprise 3 morphological types, β-catenin activation drives overproduction of primarily glial-like Type I Taste Cells in both anterior fungiform (FF) and posterior circumvallate (CV) Taste Buds, with a small increase in Type II receptor Cells for sweet, bitter and umami, but does not alter Type III sour detector Cells. Beta-catenin activation in post-mitotic Taste Bud precursors likewise regulates Cell differentiation; forced activation of β-catenin in these Shh+ Cells promotes Type I Cell fate in both FF and CV Taste Buds, but likely does so non-Cell autonomously. Our data are consistent with a model where β-catenin signaling levels within lingual epithelial progenitors dictate Cell fate prior to or during entry of new Cells into Taste Buds; high signaling induces Type I Cells, intermediate levels drive Type II Cell differentiation, while low levels may drive differentiation of Type III Cells
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mechanisms of Taste Bud Cell loss after head and neck irradiation
The Journal of Neuroscience, 2012Co-Authors: Ha M Nguyen, Mary E Reyland, Linda A. BarlowAbstract:Taste loss in human patients following radiotherapy for head and neck cancer is a common and significant problem, but the Cellular mechanisms underlying this loss are not understood. Taste stimuli are transduced by receptor Cells within Taste Buds, and like epidermal Cells, Taste Cells are regularly replaced throughout adult life. This renewal relies on progenitor Cells adjacent to Taste Buds, which continually supply new Cells to each Bud. Here we treated adult mice with a single 8 Gy dose of x-ray irradiation to the head and neck, and analyzed Taste epithelium at 1-21 d postirradiation (dpi). We found irradiation targets the Taste progenitor Cells, which undergo Cell cycle arrest (1-3 dpi) and apoptosis (within 1 dpi). Taste progenitors resume proliferation at 5-7 dpi, with the proportion of Cells in S and M phase exceeding control levels at 5-6 and 6 dpi, respectively, suggesting that proliferation is accelerated and/or synchronized following radiation damage. Using 5-bromo-2-deoxyuridine birthdating to identify newborn Cells, we found that the decreased proliferation following irradiation reduces the influx of Cells at 1-2 dpi, while the robust proliferation detected at 6 dpi accelerates entry of new Cells into Taste Buds. In contrast, the number of differentiated Taste Cells was not significantly reduced until 7 dpi. These data suggest a model where continued natural Taste Cell death, paired with temporary interruption of Cell replacement, underlies Taste loss after irradiation.
Zachary J Cohn - One of the best experts on this subject based on the ideXlab platform.
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Lipopolysaccharide-induced inflammation attenuates Taste progenitor Cell proliferation and shortens the life span of Taste Bud Cells
BMC Neuroscience, 2010Co-Authors: Zachary J Cohn, Liquan Huang, Joseph Brand, Hong WangAbstract:Background The mammalian Taste Bud, a complex collection of Taste sensory Cells, supporting Cells, and immature basal Cells, is the structural unit for detecting Taste stimuli in the oral cavity. Even though the Cells of the Taste Bud undergo constant turnover, the structural homeostasis of the Bud is maintained by balancing Cell proliferation and Cell death. Compared with nongustatory lingual epithelial Cells, Taste Cells express higher levels of several inflammatory receptors and signalling proteins. Whether inflammation, an underlying condition in some diseases associated with Taste disorders, interferes with Taste Cell renewal and turnover is unknown. Here we report the effects of lipopolysaccharide (LPS)-induced inflammation on Taste progenitor Cell proliferation and Taste Bud Cell turnover in mouse Taste tissues. Results Intraperitoneal injection of LPS rapidly induced expression of several inflammatory cytokines, including tumor necrosis factor (TNF)-α, interferon (IFN)-γ, and interleukin (IL)-6, in mouse circumvallate and foliate papillae. TNF-α and IFN-γ immunoreactivities were preferentially localized to subsets of Cells in Taste Buds. LPS-induced inflammation significantly reduced the number of 5-bromo-2'-deoxyuridine (BrdU)-labeled newborn Taste Bud Cells 1-3 days after LPS injection, suggesting an inhibition of Taste Bud Cell renewal. BrdU pulse-chase experiments showed that BrdU-labeled Taste Cells had a shorter average life span in LPS-treated mice than in controls. To investigate whether LPS inhibits Taste Cell renewal by suppressing Taste progenitor Cell proliferation, we studied the expression of Ki67, a Cell proliferation marker. Quantitative real-time RT-PCR revealed that LPS markedly reduced Ki67 mRNA levels in circumvallate and foliate epithelia. Immunofluorescent staining using anti-Ki67 antibodies showed that LPS decreased the number of Ki67-positive Cells in the basal regions surrounding circumvallate Taste Buds, the niche for Taste progenitor Cells. PCR array experiments showed that the expression of cyclin B2 and E2F1, two key Cell cycle regulators, was markedly downregulated by LPS in the circumvallate and foliate epithelia. Conclusions Our results show that LPS-induced inflammation inhibits Taste progenitor Cell proliferation and interferes with Taste Cell renewal. LPS accelerates Cell turnover and modestly shortens the average life span of Taste Cells. These effects of inflammation may contribute to the development of Taste disorders associated with infections.
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lipopolysaccharide induced inflammation attenuates Taste progenitor Cell proliferation and shortens the life span of Taste Bud Cells
BMC Neuroscience, 2010Co-Authors: Zachary J Cohn, Liquan Huang, Joseph G Brand, Agnes Kim, Hong WangAbstract:Background The mammalian Taste Bud, a complex collection of Taste sensory Cells, supporting Cells, and immature basal Cells, is the structural unit for detecting Taste stimuli in the oral cavity. Even though the Cells of the Taste Bud undergo constant turnover, the structural homeostasis of the Bud is maintained by balancing Cell proliferation and Cell death. Compared with nongustatory lingual epithelial Cells, Taste Cells express higher levels of several inflammatory receptors and signalling proteins. Whether inflammation, an underlying condition in some diseases associated with Taste disorders, interferes with Taste Cell renewal and turnover is unknown. Here we report the effects of lipopolysaccharide (LPS)-induced inflammation on Taste progenitor Cell proliferation and Taste Bud Cell turnover in mouse Taste tissues.
Hsiuni Kung - One of the best experts on this subject based on the ideXlab platform.
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arecoline alters Taste Bud Cell morphology reduces body weight and induces behavioral preference changes in gustatory discrimination in c57bl 6 mice
Chemical Senses, 2016Co-Authors: Weihau Peng, Yatpang Chau, Hsiuni KungAbstract:Arecoline, a major alkaloid in areca nuts, is involved in the pathogenesis of oral diseases. Mammalian Taste Buds are the structural unit for detecting Taste stimuli in the oral cavity. The effects of arecoline on Taste Bud morphology are poorly understood. Arecoline was injected intraperitoneally (IP) into C57BL/6 mice twice daily for 1-4 weeks. After arecoline treatment, the vallate papillae were processed for electron microscopy and immunohistochemistry analysis of Taste receptor proteins (T1R2, T1R3, T1R1, and T2R) and Taste associated proteins (α-gustducin, PLCβ2, and SNAP25). Body weight, food intake and water consumption were recorded. A 2-bottle preference test was also performed. The results demonstrated that 1) arecoline treatment didn't change the number and size of the Taste Buds or Taste Bud Cells, 2) electron microscopy revealed the change of organelles and the accumulation of autophagosomes in type II Cells, 3) immunohistochemistry demonstrated a decrease of Taste receptor T1R2- and T1R3-expressing Cells, 4) the body weight and food intake were markedly reduced, and 5) the sweet preference behavior was reduced. We concluded that the long-term injection of arecoline alters the morphology of type II Taste Bud Cells, retards the growth of mice, and affects discrimination competencies for sweet tastants.
Liquan Huang - One of the best experts on this subject based on the ideXlab platform.
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Lipopolysaccharide-induced inflammation attenuates Taste progenitor Cell proliferation and shortens the life span of Taste Bud Cells
BMC Neuroscience, 2010Co-Authors: Zachary J Cohn, Liquan Huang, Joseph Brand, Hong WangAbstract:Background The mammalian Taste Bud, a complex collection of Taste sensory Cells, supporting Cells, and immature basal Cells, is the structural unit for detecting Taste stimuli in the oral cavity. Even though the Cells of the Taste Bud undergo constant turnover, the structural homeostasis of the Bud is maintained by balancing Cell proliferation and Cell death. Compared with nongustatory lingual epithelial Cells, Taste Cells express higher levels of several inflammatory receptors and signalling proteins. Whether inflammation, an underlying condition in some diseases associated with Taste disorders, interferes with Taste Cell renewal and turnover is unknown. Here we report the effects of lipopolysaccharide (LPS)-induced inflammation on Taste progenitor Cell proliferation and Taste Bud Cell turnover in mouse Taste tissues. Results Intraperitoneal injection of LPS rapidly induced expression of several inflammatory cytokines, including tumor necrosis factor (TNF)-α, interferon (IFN)-γ, and interleukin (IL)-6, in mouse circumvallate and foliate papillae. TNF-α and IFN-γ immunoreactivities were preferentially localized to subsets of Cells in Taste Buds. LPS-induced inflammation significantly reduced the number of 5-bromo-2'-deoxyuridine (BrdU)-labeled newborn Taste Bud Cells 1-3 days after LPS injection, suggesting an inhibition of Taste Bud Cell renewal. BrdU pulse-chase experiments showed that BrdU-labeled Taste Cells had a shorter average life span in LPS-treated mice than in controls. To investigate whether LPS inhibits Taste Cell renewal by suppressing Taste progenitor Cell proliferation, we studied the expression of Ki67, a Cell proliferation marker. Quantitative real-time RT-PCR revealed that LPS markedly reduced Ki67 mRNA levels in circumvallate and foliate epithelia. Immunofluorescent staining using anti-Ki67 antibodies showed that LPS decreased the number of Ki67-positive Cells in the basal regions surrounding circumvallate Taste Buds, the niche for Taste progenitor Cells. PCR array experiments showed that the expression of cyclin B2 and E2F1, two key Cell cycle regulators, was markedly downregulated by LPS in the circumvallate and foliate epithelia. Conclusions Our results show that LPS-induced inflammation inhibits Taste progenitor Cell proliferation and interferes with Taste Cell renewal. LPS accelerates Cell turnover and modestly shortens the average life span of Taste Cells. These effects of inflammation may contribute to the development of Taste disorders associated with infections.
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lipopolysaccharide induced inflammation attenuates Taste progenitor Cell proliferation and shortens the life span of Taste Bud Cells
BMC Neuroscience, 2010Co-Authors: Zachary J Cohn, Liquan Huang, Joseph G Brand, Agnes Kim, Hong WangAbstract:Background The mammalian Taste Bud, a complex collection of Taste sensory Cells, supporting Cells, and immature basal Cells, is the structural unit for detecting Taste stimuli in the oral cavity. Even though the Cells of the Taste Bud undergo constant turnover, the structural homeostasis of the Bud is maintained by balancing Cell proliferation and Cell death. Compared with nongustatory lingual epithelial Cells, Taste Cells express higher levels of several inflammatory receptors and signalling proteins. Whether inflammation, an underlying condition in some diseases associated with Taste disorders, interferes with Taste Cell renewal and turnover is unknown. Here we report the effects of lipopolysaccharide (LPS)-induced inflammation on Taste progenitor Cell proliferation and Taste Bud Cell turnover in mouse Taste tissues.
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inflammation activates the interferon signaling pathways in Taste Bud Cells
The Journal of Neuroscience, 2007Co-Authors: Hong Wang, Minliang Zhou, Joseph G Brand, Liquan HuangAbstract:Patients with viral and bacterial infections or other inflammatory illnesses often experience Taste dysfunctions. The agents responsible for these Taste disorders are thought to be related to infection-induced inflammation, but the mechanisms are not known. As a first step in characterizing the possible role of inflammation in Taste disorders, we report here evidence for the presence of interferon (IFN)-mediated signaling pathways in Taste Bud Cells. IFN receptors, particularly the IFN-gamma receptor IFNGR1, are coexpressed with the Taste Cell-type markers neuronal Cell adhesion molecule and alpha-gustducin, suggesting that both the Taste receptor Cells and synapse-forming Cells in the Taste Bud can be stimulated by IFN. Incubation of Taste Bud-containing lingual epithelia with recombinant IFN-alpha and IFN-gamma triggered the IFN-mediated signaling cascades, resulting in the phosphorylation of the downstream STAT1 (signal transducer and activator of transcription protein 1) transcription factor. Intraperitoneal injection of lipopolysaccharide or polyinosinic:polycytidylic acid into mice, mimicking bacterial and viral infections, respectively, altered gene expression patterns in Taste Bud Cells. Furthermore, the systemic administration of either IFN-alpha or IFN-gamma significantly increased the number of Taste Bud Cells undergoing programmed Cell death. These findings suggest that bacterial and viral infection-induced IFNs can act directly on Taste Bud Cells, affecting their Cellular function in Taste transduction, and that IFN-induced apoptosis in Taste Buds may cause abnormal Cell turnover and skew the representation of different Taste Bud Cell types, leading to the development of Taste disorders. To our knowledge, this is the first study providing direct evidence that inflammation can affect Taste Buds through cytokine signaling pathways.
