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ABSTRACT: Tonsillar Tissue

PROVIDER: PRJNA818013 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18390865_1.fastq.gz	Fastqsanger.gz
	SRR18390865_2.fastq.gz	Fastqsanger.gz

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Distinct stage-specific transcriptional states of B cells in human tonsillar tissue [single-cell RNA-seq]

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Project description:Background: Tonsillectomy improves or cures symptoms in patients with palmoplantar pustulosis (PPP) and suppresses disease progression in patients with pustulotic arthro-osteitis (PAO), highlighting the important role of tonsils in the pathogenesis of PPP/PAO. Objective: To identify active inflammatory pathways in the tonsil tissue of patients with PPP/PAO, and to clarify the characteristics of tonsillar microbiota. Methods: We assessed gene expression in tonsil tissue removed from Japanese adults with PPP/PAO or recurrent tonsillitis (RT)/sleep apnea syndrome (SAS) using microarray and quantitative reverse transcription polymerase chain reaction analysis. We also performed a comprehensive analysis of the tonsillar microbiota (tonsillar crypts) using next-generation sequencing. Potential associations between tonsillar gene expression and bacterial composition were evaluated. Results: Twenty-five tonsils from patients with PPP/PAO and 15 tonsils from patients with RT/SAS were included. The gene expression of inflammatory cytokines and molecules involved in the Th17, Th2, and Treg pathways was significantly higher in the tonsillar tissue of patients with PPP/PAO than in patients with RT/SAS. There were no significant differences in genus-level tonsillar microbiota between the two groups. Correlation analysis revealed a significant positive correlation between Streptococcus spp. and the expression of Th17 and Th2 pathway genes. Correlation patterns were similar between the PPP/PAO and RT/SAS groups for Streptococcus spp. but differed for the other genera. Conclusion: The tonsils of patients with PPP/PAO are in a complex inflammatory state, with enhanced Th17, Th2, and Treg responses. Members of the Streptococcus genus may be involved in the induction of inflammatory characteristics in PPP/PAO.

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