Project description:As the first defense line to contact respiratory allergens, epithelial cells play an extremely critical role in the occurrence of allergic rhinitis, and the mechanism is realized by the regulation of the expression of co-expressed mRNA which is controlled by lncRNA. We used microarrays to screen gene expression profiles in nasal mucosal epithelial cells of allergic rhinitis, and predicted the relationship between lncRNA and mRNA by bioinformatics analysis.
Project description:Analysis of nasal epithelial cells from adult patients with seasonal allergic rhinitis and from non allergic controls. Results provide insight into the molecular mechanisms associated with inflammatory responses in nasal mucosa. Total RNA was obtained from nasal epithelial cells of 7 seasonal allergic rhinitis patients and 5 non-allergic control subjects
Project description:Analysis of nasal epithelial cells from adult patients with seasonal allergic rhinitis and from non allergic controls. Results provide insight into the molecular mechanisms associated with inflammatory responses in nasal mucosa.
Project description:Antigen uptake, processing, trafficking and presentation in nasal mucosal tissues are regulated by complex intra- and inter-cellular signalling events. Typical vaccine adjuvants lead to the transcription of pro-inflammatory cytokines and chemokines which relate to immune induction. We used microarrays to detail the global expression of genes in murine nasal mucosa underlying immune induction with a non-inflammatory nanoemulsion nasal adjuvant.
Project description:Antigen uptake, processing, trafficking and presentation in nasal mucosal tissues are regulated by complex intra- and inter-cellular signalling events. Typical vaccine adjuvants lead to the transcription of pro-inflammatory cytokines and chemokines which relate to immune induction. We used microarrays to detail the global expression of genes in murine nasal mucosa underlying immune induction with a non-inflammatory nanoemulsion nasal adjuvant. 8 week old female CD-1 mice were nasally treated with 5 microliters/nare of either 20% (v/v) naomeulsion (W805EC) or PBS. Nasal epithelium was harvested immediately post-mortem at either 6 (6 hr) or 24 hours (24 hr) following treatment. The tissue was placed in OTC and frozen by immersion in liquid nitrogen. Total RNA was extracted per sample using RNA easy (Qiagen).
Project description:To explore the impact of nasal commensal viruses on the onset and progression of allergic rhinitis, We used single cell RNA sequencing (scRNA-seq) to analyze the diversity of CD45+ cells in the nasal mucosa of control and AR mice treated with Vehicle or Ribavirin.
Project description:The aim of this study was to perform a genome-wide transcriptional analysis (mRNA + microRNA) during in vitro mucociliary differentiation of primary human basal stem/progenitors cells (BSCs) cultured at the air-liquid interface (ALI) system. We used microarrays to detail the global gene expression underlying mucociliary differentiation of human upper airways basal stem/progenitor cells isolated from nasal polyps and control nasal mucosa.
Project description:Nasal mucosa and olfactory bulb are separated by the cribriform plate which is perforated by olfactory nerves. We have previously demonstrated that the cribriform plate is permissive for T cells and monocytes and that viruses can enter the bulb upon intranasal injection by axonal transportation. Therefore, we hypothesized that nasal mucosa and olfactory bulb are equipped to deal with constant infectious threats. To detect genes involved in this process, we compared gene expression in nasal mucosa and bulb of mice kept under specific pathogen free (SPF) conditions to gene expression of mice kept on non-SPF conditions using RNA deep sequencing. We found massive alterations in the expression of immune-related genes of the nasal mucosa, while the bulb did not respond immunologically. The absence of induction of immune-related genes in the olfactory bulb suggests effective defence mechanisms hindering entrance of environmental pathogens beyond the outer arachnoid layer. The genes detected in this study may include candidates conferring susceptibility to meningitis.