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Bitter taste receptors, also known as type 2 taste receptors (T2Rs), are found not only in the mouth's taste bud cells but also in various tissues and cells, including macrophages. Macrophages, known for their remarkable plasticity, play a crucial role in regulating innate immunity, managing inflammation, and orchestrating immune responses to antigens, pathogens, and environmental factors. Recently, the study of the expression and function of bitter taste receptors within macrophages has garnered significant interest. This review summarizes the expression levels and distribution characteristics of bitter taste receptors in macrophages and examines their effects on macrophage polarization, phagocytosis, and chemotaxis, as well as their potential molecular mechanisms. The purpose of this review is to provide insight and perspectives for research on the regulatory role of T2Rs in macrophage functions. [ABSTRACT FROM AUTHOR]

Capsaicin is an active ingredient that characterizes the pungency of pepper, and is the key to the 'door of spicy sensation', that is, the source of spicy sensation. Through the interaction with the oral cavity, capsaicin substances make TRPV1 activated by capsaicin, increase intracellular calcium ions, trigger nerve endings, release neuropeptides, and finally cause the formation of pain sensation in the cerebral cortex, thus generating a spicy sensation. It has been found that capsaicin has certain damage to taste. Capsaicin may directly or indirectly inhibit the transmission of taste nerve by reducing the number of taste buds and changing the excitability of taste transduction or taste receptor cells, thus causing damage to relevant taste cells and nerves. This paper summarizes the regulation and damage mechanism of capsaicin to taste and the research status of the new capsaicin taste interaction technology, discusses the shortcomings of its potential influence mechanism, and looks forward to the future research direction, in order to provide reference for the application of capsaicin in food and the prevention of damage caused by capsaicin. [ABSTRACT FROM AUTHOR]

BACKGROUND: Gingiva is one of key components in periodontal complex, which is characterized by wound healing without scar. Gingival mesenchymal stem cells have multi-directional differentiation potential. In recent years, more and more studies have demonstrated that Gingival mesenchymal stem cells can be applied in the regeneration of certain tissues. OBJECTIVE: To review the researches of gingival mesenchymal stem cells in tissue regeneration. METHODS: Retrieval of related-articles in nearly 20 years was conducted via China Biology Medicine (CBM), CNKI, PubMed databases. The search terms included “gingiva, mesenchymal stem cells, stem cell, regeneration, tissue, scaffold”. After preliminary screening through reading titles and abstracts to exclude the articles that were not related to the topic, 60 articles were finally included for further analysis. RESULTS AND CONCLUSION: (1) Gingival mesenchymal stem cells can be differentiated into osteoblasts, chondroblasts, lipoblasts, endothelial cells, auditory cells and taste bud cells under certain induction conditions in vitro. (2) The combination of gingival mesenchymal stem cells and scaffolds such as alginate 3D scaffolds, 3D-printed polylactic acid scaffolds and 3D collagen scaffolds, can enhance the tissue regeneration potential. (3) Bioactive factors such as dexamethasone, bone-specific growth factor and insulin-like growth factor, can also enhance the regenerative potential. (4) However, the current construction and preparation of scaffold to delivery gingival mesenchymal stem cells are not ideal such as low survival rate and differentiation rate. Future research should focus on how to improve the efficiency of scaffold in order to apply gingival mesenchymal stem cells to regenerate tissue in clinic. [ABSTRACT FROM AUTHOR]

Copyright of West China Journal of Stomatology is the property of Sichuan University, West China College of Stomatology and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Shipin Kexue/ Food Science is the property of Food Science Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Food Research & Development is the property of Food Research & Development Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of West China Journal of Stomatology is the property of Sichuan University, West China College of Stomatology and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

BACKGROUND: Fungiform and circumvallate papillas on the surface of the mammal tongue mucosa are mainly associated with taste. Taste abnormalities seriously affect patients' quality of life, so it is of significance to understand the developmental processes of fungiform papilla and taste buds, for hypogeusia treatment. OBJECTIVE: To observe the morphological changes of mouse tongue fungiform papilla and taste buds during their developmental processes. METHODS: The tongues of C57BL/6J mice were observed by scanning electron microscope and hematoxylin eosin staining at embryonic days 13.5-18.5 (E13.5-E 18.5), postnatal (PN) days 0.5, 4.5, 7.5, 14.5, 21.5, 90.5, and postnatal 1.5 years (PN1.5Y), and Shh antibody was used for immunohistochemical staining. Immunohistochemical staining of S-100 was performed on the tongue specimens of the mice at E16.5 and E18.5. RESULTS AND CONCLUSION: The number of fungiform papilla was mainly determined at E13.5-E14.5. From E15.5, the papilla gradually matured in morphology. Taste bud development began at E16.5, and the taste pore began to form at PN7.5. In adult and old age, taste bud cells and intercellular substances were reduced, and keratosis surrounding the fungiform papillae was visible. Shh was expressed in the epithelial cells of fungiform papilla at E14.5, in the epithelial cells at the tip of the fungiform papilla at E16.5 and E18.5, and in adult and elderly taste bud cells. These results suggest that Shh plays an important role in the development, maturation and maintenance of fungiform papillae and taste buds. S-100 is expressed in the connective tissue beneath the fungiform papillae at E18.5, indicating that the nerve extension may be involved in the development and maturation of taste buds. [ABSTRACT FROM AUTHOR]

The taste buds in the human tongue contain specialized cells that generate taste signals when they are stimulated. These signals are then transmitted to the central nervous system, allowing the human body to distinguish nutritious substances from toxic or harmful ones. This process is critical to the survival of humans and other mammals. A number of studies have shown that dysgeusia, or taste disorder, is a common complication of coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, which can severely affect patients' nutritional intake and quality of life. Based on the physiological process of taste perception, the direct causes of dysgeusia include dysfunction of taste receptors and damage to the taste nervous system, while indirect causes include genetic factors, aging-related changes, bacterial and viral infections, and cancer treatments such as radiotherapy and chemotherapy. The pathogenic factors of dysgeusia are complicated, further research is needed to fully understand the underlying mechanisms, and some of the reported findings and conclusions still need further validation. All these form a great challenge for clinical diagnosis of the cause and targeted treatment of dysgeusia. Herein, we reviewed published research on the physiological process of taste perception, the potential mechanisms of taste disorders related to SARS-CoV-2 infection, and strategies for prevention and treatment, providing theoretical support for establishing and improving the comprehensive management of COVID-19 complicated by taste disorders., (Copyright© by Editorial Board of Journal of Sichuan University (Medical Sciences).)

Objectives: To identify the alternative splicing isoform of mouse sweet taste receptor T1R2, and investigate the effect of lipopolysaccharide (LPS) local injection on T1R2 alternative splicing and the function of sweet taste receptor as one of the bacterial virulence factors., Methods: After mouse taste bud tissue isolation was conducted, RNA extraction and reverse transcription polymerase chain reaction (PCR) were performed to identify the splicing isoform of T1R2. Heterologous expression experiments in vitro were utilized to detect how the T1R2 isoform regulated the function of sweet taste receptors. The effect of local LPS injection on the expression of the T1R2 isoform was measured by real-time fluorescent quantitative PCR., Results: T1R2 splicing isoform T1R2_Δe3p formed sweet taste receptors with T1R3, which could not be activated by sweet taste stimuli and significantly downregulated the function of canonical T1R2/T1R3. Local LPS injection significantly increased the expression ratio of T1R2_Δe3p in mouse taste buds., Conclusions: LPS stimulation affects the alternative splicing of mouse sweet taste receptor T1R2 and significantly upregulates the expression of non-functional isoform T1R2_Δe3p, suggesting that T1R2 alternative splicing regulation may be one of the mechanisms by which microbial infection affects host taste perception.

Objective: To observe the effect of electroacupuncture (EA) on food intake, body weight, number of taste bud cells and the expression of lipid taste bud receptor (CD36), Gα-gustducin, post-synaptic density protein 95 (PSD95) and neurofilament light chain (NFL) proteins in the tongue or hippocampus in obese rats, so as to explore its mechanism underlying reducing body weight., Methods: A total of 30 male SD rats were randomly divided into control, model and EA groups ( n =10 in each group, 5 rats for H.E. staining and immunohistochemistry, and 5 for Western blot). The obesity model was established by feeding the rats with high fat diet for 11 weeks. Following successful modeling, EA (2 Hz/15 Hz, 1.0-1.2 mA) was applied to "Tianshu" (ST25) for 30 min, once a day, 5 times/week for 5 weeks. The body length, body weight and maximum daily food consumption were recorded every day, followed by calculating the lee's index. Histopathological changes of the circumvallate papillae (CVP) and number of taste bud cells and CD36 were detected by HE staining and immunohistochemistry (IHC), separately. The expression levels of CD36, PSD95 and NFL proteins in the hippocampus were detected by Western blot., Results: The body weight, Lee's index and daily food consumption were significantly higher in the model group than in the control group ( P <0.01), and were significantly lowered after EA intervention in comparison with the model group ( P <0.01), suggesting an improvement of obesity. H.E. staining displayed that the CVP area and the number of taste bud cells were obviously decreased in the model group in contrast to the control group ( P <0.01), and were notably increased in the EA group in contrast to the model group ( P <0.05, P <0.01). IHC and Western blot showed that the expression levels of CD36 in the tongue and hippocampus were obviously up-regulated in the model group relevant to the control group ( P <0.01, P <0.05), and considerably down-regulated in the EA group relevant to the model group ( P <0.05, P <0.01). The expression levels of Gα-gustducin in the tongue, and PSD95 and NFL in the hippocampus were remarkably decreased in the model group relevant to the control group ( P <0.01, P <0.05), and significantly increased in the EA group relevant to the model group ( P <0.01, P <0.05)., Conclusion: EA can reduce daily food consumption and body weight in obese rats, which is associated with its effects in down-regulating the expression of CD36 in taste buds and hippocampus, and up-regulating the expression of Gα-gustducin in the tongue, and PSD95 and NFL proteins in the hippocampus. It suggests that EA may regulate the feeding behavior of obese rats by influencing the cognitive memory mechanism involved in CD36 in hippocampus.

Taste is mediated by multicellular taste buds distributed throughout the oral and pharyngeal cavities. The taste buds can detect five basic tastes: sour, sweet, bitter, salty and umami, allowing mammals to select nutritious foods and avoid the ingestion of toxic and rotten foods. Once developed, the taste buds undergo continuous renewal throughout the adult life. In the past decade, significant progress has been achived in delineating the cellular and molecular mechanisms governing taste buds development and homeostasis. With this knowledges and in-depth investigations in the future, we can achieve the precise management of taste dysfunctions such as dysgeusia and ageusia.

Taste receptors guide individuals to consume nutrients while avoiding potentially noxious substances. Interestingly, recent studies have shown that taste receptors are also expressed beyond the taste buds, including brain, respiratory system, and digestive system, etc. These extragustatory taste receptors play important roles in microbial infection, nutrient uptake and host homeostasis. Mang extragustatory taste receptors have been proposed to sense microorganisms and regulate host innate defense. More importantly, polymorphisms of genes encoding taste receptor, particularly bitter taste receptor, are linked to different innate defensive responses. This review introduces the molecular basis of taste signal transduction, and the role of taste receptors in the regulation of innate immunity during microbial infection were further discussed in detail.

Objective: To compare characterization of microRNAs (miRNAs) expression profiles of induced pluripotent stem cells (iPSCs) reprogrammed from human dental pulp stem cells (DPSCs) and stem cells from apical papilla (SCAP) and screen-specific microRNA., Methods: Human DPSCs and SCAP were reprogrammed into iPSCs using a Sendai virus vector. Total RNA of human DPSCs-iPSCs and SCAP-iPSCs were extracted. miRNAs were labeled and hybridized. Slides were scanned, and images were imported into GenePix Pro 6.0 for grid alignment and data extraction. Significant differentially expressed miRNAs between the two groups were identified using fold change and P-value and were analyzed., Results: Both human DPSCs and SCAP were successfully reprogrammed into iPSCs. Among miRNA genes analyzed by miRNA microarray, 68 were differentially expressed by more than 10-fold in DPSCs-iPSCs; 37 of these genes were up-regulated, and 31 were down-regulated. In SCAP-iPSCs, 107 genes were differentially expressed by more than 10-fold; 68 were up-regulated, and 39 were down-regulated. In both cells, only miR-302e was up-regulated, whereas 9 miRNAs were down-regulated: miR-29b-3p, miR-181b-5p, miR-4328, miR-22-5p, miR-145-5p, miR-4324, let-7b-5p, miR-181a-5p, and miR-27b-3p., Conclusions: Multiple miRNAs participated in reprogramming of human DPSCs and SCAP into iPSCs. Most miRNAs are related to cell cycle, transforming growth factor-β signaling pathways and epithelial-mesenchymal transition.