MicroRNA Expression Patterns of CD8+ T Cells in Acute and Chronic Brucellosis

PLoS One. 2016 Nov 8;11(11):e0165138. doi: 10.1371/journal.pone.0165138. eCollection 2016.

Abstract

Although our knowledge about Brucella virulence factors and the host response increase rapidly, the mechanisms of immune evasion by the pathogen and causes of chronic disease are still unknown. Here, we aimed to investigate the immunological factors which belong to CD8+ T cells and their roles in the transition of brucellosis from acute to chronic infection. Using miRNA microarray, more than 2000 miRNAs were screened in CD8+ T cells of patients with acute or chronic brucellosis and healthy controls that were sorted from peripheral blood with flow cytometry and validated through qRT-PCR. Findings were evaluated using GeneSpring GX (Agilent) 13.0 software and KEGG pathway analysis. Expression of two miRNAs were determined to display a significant fold change in chronic group when compared with acute or control groups. Both miRNAs (miR-126-5p and miR-4753-3p) were decreased (p <0.05 or fold change > 2). These miRNAs have the potential to be the regulators of CD8+ T cell-related marker genes for chronic brucellosis infections. The differentially expressed miRNAs and their predicted target genes are involved in MAPK signaling pathway, cytokine-cytokine receptor interactions, endocytosis, regulation of actin cytoskeleton, and focal adhesion indicating their potential roles in chronic brucellosis and its progression. It is the first study of miRNA expression analysis of human CD8+ T cells to clarify the mechanism of inveteracy in brucellosis.

MeSH terms

  • Acute Disease
  • Adult
  • Brucellosis / metabolism*
  • CD8-Positive T-Lymphocytes / metabolism*
  • Chronic Disease
  • Disease Progression
  • Female
  • Gene Expression Profiling / methods
  • Host-Pathogen Interactions / physiology
  • Humans
  • Immune Evasion / physiology
  • Male
  • MicroRNAs / metabolism*
  • Middle Aged
  • Signal Transduction / physiology

Substances

  • MicroRNAs

Grants and funding

This work was supported by the grant from Uludag University, Bursa, Turkey (grant number UAP(T)‐2011/15).