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Transcriptome Profiling Reveals Indoxyl Sulfate Should Be Culpable of Impaired T Cell Function in Chronic Kidney

Fangfang Xiang1,2,3, Xuesen Cao1, Bo Shen1

  • 1Department of Nephrology, Zhongshan Hospital, Fudan University, Shanghai, China.

Frontiers in Medicine
|May 22, 2020
PubMed

Insights

Indoxyl sulfate (IS), a uremic toxin, triggers chronic inflammation and DNA damage in T cells, potentially explaining complications in chronic kidney disease (CKD). This study reveals IS impacts T cell gene expression and function.

Area of Science:

  • Immunology
  • Nephrology
  • Toxicology

Background:

  • Chronic inflammation and immune dysfunction are key in chronic kidney disease (CKD) pathogenesis.
  • Uremic toxins, like indoxyl sulfate (IS), are implicated as a "missing link" in CKD complications.
  • The impact of IS on immune cell function, specifically T cells, remained largely unstudied.

Purpose of the Study:

  • To investigate the genome-wide gene expression profile of human peripheral T cells stimulated by IS.
  • To identify differentially expressed genes (DEGs) and understand IS's effects on T cell function.
  • To explore the role of IS as an endogenous ligand for the Aryl hydrocarbon receptor (AhR).

Main Methods:

  • RNA-sequencing transcriptome profiling of human peripheral T cells treated with IS in vitro.
  • Identification of differentially expressed genes (DEGs) in response to IS.
  • Validation of key findings using flow cytometry and western blot analysis.

Main Results:

  • Over 5129 DEGs were identified, with significant up- or down-regulation by IS, some concentration-specific.
  • IS stimulation altered T cell functional markers and transcription factor profiles.
  • IS upregulated Aryl hydrocarbon receptor (AhR) target genes and pro-inflammatory cytokines (TNF-α, IFN-γ), inducing DNA damage in T cells.

Conclusions:

  • IS exhibits toxicity to T cells, contributing to chronic inflammation in CKD.
  • As an AhR ligand, IS influences T cell inflammatory response and cell cycle regulation.
  • Further research is needed to elucidate mechanisms and develop strategies to preserve T cell function in CKD.
Keywords:
RNA-sequencingT cellaryl hydrocarbon receptorchronic kidney diseaseindoxyl sulfate

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