Inhibition of TLR8 mediated signaling promotes BCG induced apoptosis in THP-1 cells

Microb Pathog. 2016 Apr:93:78-82. doi: 10.1016/j.micpath.2015.11.028. Epub 2015 Nov 30.

Abstract

Apoptosis was considered as one of the important host defense mechanisms against mycobacteria infection. In macrophage, the main target cell of Mycobacterium tuberculosis, apoptosis after infection could help kill the bacillus inside and process the antigens for further presentation and proper immune response. Here, we identified a role of TLR8 during the apoptosis induced by Bacillus Calmette Guérin (BCG) infection in THP-1 cells. Knockdown TLR8 further increased the apoptosis induced by BCG infection, and this enhanced apoptosis was caspase-dependent. During this process, Erk1/2, JNK and NFκB pathways were negatively affected and contributed to the enhanced apoptosis.

Keywords: Apoptosis; Bacillus Calmette Guérin; Mycobacterium; TLR8.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis*
  • Cattle
  • Cell Line
  • Macrophages / cytology*
  • Macrophages / metabolism
  • Macrophages / microbiology
  • Mycobacterium bovis / genetics
  • Mycobacterium bovis / physiology*
  • Signal Transduction
  • Toll-Like Receptor 1 / genetics
  • Toll-Like Receptor 1 / metabolism*
  • Tuberculosis, Bovine / genetics
  • Tuberculosis, Bovine / metabolism*
  • Tuberculosis, Bovine / microbiology
  • Tuberculosis, Bovine / physiopathology*

Substances

  • Toll-Like Receptor 1