Dataset Information

Deciphering the resiquimod induced toll-like receptor signalling pathway in chickens

ABSTRACT: Resiquimod (R-848) is a synthetic TLR7 agonist. This study was targeted to understand the signaling molecules involved in the Resiquimod (R-848) mediated TLR7 stimulation in the chicken and specifically for Th1 and Th2 type of immune responses. For this, transcriptome data (RNA-seq) was generated from RNA extracted at 24 hour from spleen tissues (1 each) of both control (untreated) and chicken administered with R-848 (intra muscular route). Upregulated and downregulated genes were identified following using transcriptome analysis pipeline Geo2RNAseq_0.99.9 (https://anaconda.org/xentrics/r-geo2rnaseq). Within the pipeline, the reads were quality checked using FastQC, quality trimming performed with Trimmomatic (Bolger et al., 2014) and reference genome (Gallus gallus: GRCg6a (GCA_000002315.5)) mapping was carried out using TopHat2 (Kim et al., 2013). Differently expressed genes (DEGs) were identified using baySeq (Hardcastle and Kelly, 2010). Functional annotation of DEGs were carried out using g:Profiler (Reimandet al., 2016; http://biit.cs.ut.ee/gprofiler/). Among the 5884 DEG, eight genes enriched in biological processes associated to signal transduction (MAPK14, MAP3K8, PIK3CD, STAT1, STAT3, MAPK11 LRRK2, and GATA3) were considered for further validation. Among the eight significant DEGs, MAPK14, MAP3K8, PIK3CD, STAT1 and STAT3 were up-regulated while MAPK11, LRRK2 and GATA3 transcripts were down-regulated in the R-848 treated birds evidenced by transcriptomic data.

ORGANISM(S): Gallus gallus

PROVIDER: GSE180434 | GEO | 2023/01/03

REPOSITORIES: GEO

ACCESS DATA

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Project description:Resiquimod is a nucleoside analog belonging to the imidazoquinoline family of compounds which is known to signal through Toll-like receptor 7. Resiquimod treatment has been demonstrated to inhibit the development of allergen induced asthma in experimental models. Despite this demonstrated effectiveness, little is known about the molecular events responsible for this effect. The aim of the present study was to elucidate the molecular processes which were altered following resiquimod treatment and antigen challenge in a mouse model of allergic asthma. Employing microarray analysis, we have characterized the 'asthmatic' transcriptome of the murine lung and determined that it includes genes involved in: the control of cell cycle progression, airway remodelling, the complement and coagulation cascades, and chemokine signalling. We have demonstrated that systemic resiquimod administration resulted in the recruitment of NK cells to the lungs of the mice, although no causal relationship between NK cell recruitment and treatment efficacy was found. Furthermore, results of our studies demonstrated that resiquimod treatment resulted in the normalization of the expression of genes involved with airway remodelling and chemokine signalling, and in the modulation of the expression of genes including cytokines and chemokines, adhesion molecules, and B-cell related genes, involved in several aspects of immune function and antigen presentation. Overall, our findings identified several genes, important in the development of asthma pathology, that were normalized following resiquimod treatment thus improving our understanding of the molecular consequences of resiquimod treatment in the lung milieu. Experiment Overall Design: A total of 18 samples, from 6 sets of biological replicates, were analyzed. 9 A/J and 9 C57BL/6 mice were divided into three equal groups. All animals were sensitized to ovalbumin, one group received PBS aerosol challenges, the other two received 1% ovalbumin aerosol challenges. Of the two ovalbumin challenged groups, one recieved resiquimod 24hours before each challenge.

Dataset Information

Deciphering the resiquimod induced toll-like receptor signalling pathway in chickens

Dataset's files

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure