Project description:We report the RNA expression using RNAseq in tongue tissue of mice with and without infection with oropharyngeal candidiasis. CCL28 KO mice are compared to C57BL/6 WT mice.
Project description:Candida albicans, the causative agent of mucosal infections including oropharyngeal candidiasis (OPC) as well as bloodstream infections is becoming increasingly resistant to existing treatment options. In the absence of novel drug candidates, drug repurposing aimed at using existing drugs to treat off label diseases is a promising strategy. C. albicans requires environmental iron for survival and virulence while host nutritional immunity deploys iron-binding proteins to sequester iron and reduce fungal growth. Here we evaluated the role of iron-limitation using Deferasirox (an FDA approved iron chelator for treatment of patients with iron overload) during murine OPC; and assessed Deferasirox-treated C. albicans for its interaction with human oral epithelial (OE), neutrophils, and antimicrobial peptides. Therapeutic Deferasirox treatment significantly reduced salivary iron levels while a non-significant reduction in fungal burden was observed. Preventive treatment that allowed for two additional days of drug administration in our murine model, resulted in significant reduction of C. albicans colony forming units (CFU)/g of tongue tissue, a significant reduction in salivary iron levels, and significantly reduced neutrophil-mediated inflammation. C. albicans harvested from tongues of animals undergoing preventive treatment had differential expression of 106 genes, including those involved in iron metabolism, adhesion, and response to host innate immunity. Moreover, Deferasirox-treated C. albicans cells had two-fold reduction in survival in neutrophil phagosomes (with greater susceptibility to oxidative stress); and reduced adhesion and invasion of OE cells, in vitro. Thus Deferasirox treatment has the potential to alleviate OPC by affecting C. albicans gene expression and reducing virulence
Project description:The ability to taste is critical for animal nutrition and toxin deterrence. The majority of research on taste bud development and regeneration is in mice, where taste buds are located within specialized papillae on the tongue. However, taste buds in fish and amphibians, such as axolotls (Ambystoma mexicanum), are not housed in papillae, rather they are within the pharyngeal epithelium. This simplified tissue level organization, along with the ability of cultured oropharyngeal explants from early embryos to produce taste buds on the same time-line as embryos, make the axolotl an excellent model to identify molecules specifically involved in taste bud cell differentiation. In this study, we performed de novo transcriptomic analysis on RNA sequences from three different stages of oropharyngeal explants: stages 37/38, 39, and 41. RNA-seq data from 17 total samples representing these stages were pooled to generate de novo assemblie(s) of the transcriptome using a Trinity pipeline. Raw reads and the assembly were uploaded to Mendeley (doi:10.17632/tvxh3jm83m.1). From 27.9Gb of raw sequences, we identified 21,244 transcripts. To our knowledge, this study provides the first published assembly of axolotl oropharyngeal endoderm explants. This RNA-seq data and transcriptome assembly provide information on genes expressed in the oropharyngeal endoderm and will be valuable in the identification of taste bud development genes.
Project description:In this study present here, we established RA-induced tongue abnormal mice model, muscle samples acquired from the tongue body and genioglossus of fetuses on E15.5 was used to get differently expressed miRNA in RA-induced group, then validated by qRT-PCR, futher analysis was conducted by bioinformatics method.
Project description:Tongue squamous cell carcinoma is a tumour type with rather low five year survival, around 60%. The poor survival rate has been ascribed to late detection, a high frequency of locoregional recurrence, the occurrence of secondary primary tumours and death due to comorbidity. One reason for development of recurrence is thought to be the existence of transformed cells in areas adjacent to the primary tumour, cancerization field effect. The aim of this study was to map the changes in the tumour free tongue tissue adjacent to tongue tumours compared with healthy control tongue tissue to better understand the cancerization field effect. Tissue biopsies were collected from tumour (T) and tumour free tissue adjacent to the tumour (TF) from patients with tongue squamous cell carcinoma. Control tissue was collected from latter border of the tongue of tumour free healthy volunteers (C). All samples were homogenized and RNA was extracted. The RNA was biotin labelled and run on Illumina HT-12 bead chip array.
Project description:This SuperSeries is composed of the following subset Series: GSE34105: Gene expression profiling of archival tongue carcinoma and normal tongue tissue (all samples) GSE34106: Gene expression profiling of archival tongue carcinoma and normal tongue tissue (subset) Refer to individual Series
Project description:The overall goal of this project is to investigate the role of TGF-beta signaling in tongue development in order to study the contribution of cranial neural crest (CNC) cells towards the patterning of cranial mesoderm for proper tongue formation. Here, we conducted gene expression profiling of embryonic tongue tissue from wild type mice as well as those with a neural crest specific conditional inactivation of the Tgfbr2 gene. The latter mice provide a model of microglossia, a common congenital birth defect which is frequently observed with several syndromic conditions. To investigate the mechanism of microglossia resulting from dysfunctional TGF-Beta signaling during muscle development, we analyzed neural crest specific conditional inactivation of Tgfbr2 in mice (Tgfbr2fl/fl;Wnt1-Cre). We performed microarray analyses of tongue tissue of Tgfbr2fl/fl;Wnt1-Cre mutant mice and Tgfbr2fl/fl control mice at embryonic day E14.5 (n=3 per genotype) to examine the genes regulated by Tgf-beta during tongue muscle development.
Project description:Nine groups of rat tongue tissue RNA samples, including three from normal control, three from 4NQO induced tongue tissue, and three from 4NQO induced and IL-1Ra interference tongue tissue (3 rats per group) were collected for gene microarray hybridization.